Hypertensive Heart Disease
Content
Hypertensive Heart Disease
Cardiovascular effects of hypertension
Uncontrolled and prolonged elevation of BP can lead to a variety of changes in the myocardial
structure, coronary vasculature, and conduction system of the heart. These changes in turn can
lead to the development of left ventricular hypertrophy (LVH), coronary artery disease (CAD),
various conduction system diseases, and systolic and diastolic dysfunction of the myocardium,
complications that manifest clinically as angina or myocardial infarction, cardiac arrhythmias
(especially atrial fibrillation), and congestive heart failure (CHF).
Thus, hypertensive heart disease is a term applied generally to heart diseases, such as coronary
artery disease, cardiac arrhythmias, and CHF, that are caused by the direct or indirect effects of
elevated BP. Although these diseases generally develop in response to chronically elevated BP,
marked and acute elevation of BP can lead to accentuation of an underlying predisposition to any
of the symptoms traditionally associated with chronic hypertension.
Etiology
The etiology of hypertensive heart disease is a complex interplay of various hemodynamic,
structural, neuroendocrine, cellular, and molecular factors. These factors play integral roles in the
development of hypertension and its complications; however, elevated BP it self can modulate
these factors.
Obesity has been linked to hypertension and LVH in various epidemiologic studies, with as
many as 50% of obese patients having some degree of hypertension and as many as 60-70% of
patients with hypertension being obese.
Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly, by
increased afterload, and indirectly, by associated neurohormonal and vascular changes. Elevated
24-hour ambulatory BP and nocturnal BP have been demonstrated to be more closely related to
various cardiac pathologies, especially in black persons. The pathophysiologies of the various
cardiac effects of hypertension differ and are described in this section.
Left ventricular hypertrophy
LVH, defined as an increase in the mass of the left ventricle, is caused by the response of
myocytes to various stimuli accompanying elevated BP. Myocyte hypertrophy can occur as a
compensatory response to increased afterload. Mechanical and neurohormonal stimuli
accompanying hypertension can lead to activation of myocardial cell growth, gene expression (of
which some occurs primarily in fetal cardiomyocytes), and, thus, to LVH.
In addition, activation of the renin-angiotensin system, through the action of angiotensin II on
angiotensin I receptors, leads to growth of interstitium and cell matrix components. In summary,
the development of LVH is characterized by myocyte hypertrophy and by an imbalance between
the myocytes and the interstitium of the myocardial skeletal structure.
Various patterns of LVH have been described, including concentric remodeling, concentric LVH,
and eccentric LVH. Concentric LVH is an increase in LV thickness and LV mass with increased
LV diastolic pressure and volume, commonly observed in persons with hypertension; this is a
marker of poor prognosis in these patients. Compare concentric LVH with eccentric LVH, in
which LV thickness is increased not uniformly but at certain sites, such as the septum.
Although the development of LVH initially plays a protective role in response to increased wall
stress to maintain adequate cardiac output, it later leads to the development of diastolic and,
ultimately, systolic myocardial dysfunction.
Left atrial abnormalities
Frequently underappreciated, structural and functional changes of the left atrium are very
common in patients with hypertension. The increased afterload imposed on the LA by the
elevated LV end-diastolic pressure secondary to increased BP leads to impairment of the left
atrium and left atrial (LA) appendage function, plus increased LA size and thickness.
Increased LA size accompanying hypertension in the absence of valvular heart disease or systolic
dysfunction usually implies chronicity of hypertension and may correlate with the severity of LV
diastolic dysfunction.
In addition to LA structural changes, these patients are predisposed to atrial fibrillation. Atrial
fibrillation, with loss of atrial contribution in the presence of diastolic dysfunction, may
precipitate overt heart failure.
Valvular disease
Although valvular disease does not cause hypertensive heart disease, chronic and severe
hypertension can cause aortic root dilatation, leading to significant aortic insufficiency. Some
degree of hemodynamically insignificant aortic insufficiency is often found in patients with
uncontrolled hypertension. An acute rise in BP may accentuate the degree of aortic insufficiency,
with return to baseline when the BP is better controlled. In addition to causing aortic
regurgitation, hypertension is also thought to accelerate the process of aortic sclerosis and cause
mitral regurgitation.
Heart failure
Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart
failure develops, the dysfunctioning left ventricle is unable to generate the high BP, thus
obscuring the heart failure's etiology. The prevalence of asymptomatic diastolic dysfunction in
patients with hypertension and without LVH may be as high as 33%. Chronically elevated
afterload and the resulting LVH can adversely affect the active early relaxation phase and the late
compliance phase of ventricular diastole.
Diastolic dysfunction
Diastolic dysfunction is common in persons with hypertension. It is often, but not invariably,
accompanied by LVH. In addition to elevated afterload, other factors that may contribute to the
development of diastolic dysfunction include coexistent coronary artery disease, aging, systolic
dysfunction, and structural abnormalities such as fibrosis and LVH. Asymptomatic systolic
dysfunction usually follows.
Systolic dysfunction
Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the
face of elevated BP, and the LV cavity begins to dilate to maintain cardiac output. As the disease
enters the end stage, LV systolic function decreases further. This leads to further increases in
activation of the neurohormonal and renin-angiotensin systems, leading to increases in salt and
water retention and increased peripheral vasoconstriction. Eventually, the already compromised
LV is overwhelmed, and the patient progresses to the stage of symptomatic systolic dysfunction.
Decompensation
Apoptosis, or programmed cell death, stimulated by myocyte hypertrophy and the imbalance
between its stimulants and inhibitors, is considered to play an important part in the transition
from compensated to decompensated stage. The patient may become symptomatic during the
asymptomatic stages of the LV systolic or diastolic dysfunction, owing to changes in afterload
conditions or to the presence of other insults to the myocardium (eg, ischemia, infarction). A
sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV
ejection fraction.
Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds
rapid deterioration in clinical status and a markedly increased risk of death. In addition to LV
dysfunction, right ventricular (RV) thickening and diastolic dysfunction also develop as results of
septal thickening and LV dysfunction.
Myocardial ischemia
Patients with angina have a high prevalence of hypertension. Hypertension is an established risk
factor for the development of coronary artery disease, almost doubling the risk. The development
of ischemia in patients with hypertension is multifactorial.
Importantly, in patients with hypertension, angina can occur in the absence of epicardial
coronary artery disease. The reason for this is 2-fold. Increased afterload secondary to
hypertension leads to an increase in LV wall tension and transmural pressure, compromising
coronary blood flow during diastole. In addition, the microvasculature beyond the epicardial
coronary arteries has been shown to be dysfunctional in patients with hypertension, and it may be
unable to compensate for increased metabolic and oxygen demand.
The development and progression of arteriosclerosis, the hallmark of coronary artery disease, is
exacerbated in arteries subjected to chronically elevated BP. Shear stress associated with
hypertension and the resulting endothelial dysfunction cause impairment in the synthesis and
release of the potent vasodilator nitric oxide. A decreased nitric oxide level promotes the
development and acceleration of arteriosclerosis and plaque formation. Morphologic features of
the plaque are identical to those observed in patients without hypertension.
Cardiac arrhythmias
Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation,
premature ventricular contractions (PVCs), and ventricular tachycardia (VT).[7] The risk of
sudden cardiac death is increased.[8] Various mechanisms thought to play a part in the
pathogenesis of arrhythmias include altered cellular structure and metabolism, inhomogeneity of
the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these
may lead to an increased risk of ventricular tachyarrhythmias.
Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in
patients with hypertension.[9] In fact, elevated BP is the most common cause of atrial fibrillation
in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had
hypertension. Although the exact etiology is not known, LA structural abnormalities, associated
coronary artery disease, and LVH have been suggested as possible contributing factors. The
development of atrial fibrillation can cause decompensation of systolic and, more importantly,
diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of
thromboembolic complications, most notably stroke.
Premature ventricular contractions, ventricular arrhythmias, and sudden cardiac death are
observed more often in patients with LVH than in those without LVH. The etiology of these
arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis.
Physical Examination
Physical signs of hypertensive heart disease depend on the predominant cardiac abnormality and
the duration and severity of the hypertensive heart disease. Findings from the physical
examination may be entirely normal in the very early stages of the disease, or the patient may
have classic signs upon examination.
Pulses
The arterial pulses are normal in the early stages of hypertensive heart disease. The cardiac
rhythm is regular if the patient is in sinus rhythm; it is irregularly irregular if the patient is in
atrial fibrillation. The heart rate is as follows:
Normal in patients in sinus rhythm
Not normal in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial fibrillation and a
rapid ventricular response
The pulse volume is usually normal, but it is decreased in patients with LV dysfunction.
Additional findings may include radial-femoral delay if the etiology of hypertension is
coarctation of the aorta
Blood pressure
Systolic and/or diastolic BP is elevated (>140/90mm Hg). Mean BP and pulse pressure are also
elevated generally. The BP in the upper extremities may be higher than that in the lower
extremities in patients with coarctation of the aorta. BP may be normal at the time of evaluation
if the patient is on adequate antihypertensive medications or if the patient has advanced LV
dysfunction and the LV cannot generate enough stroke volume and cardiac output to produce an
elevated BP.
Veins
In patients with heart failure, the jugular veins may be distended. The predominant waves depend
on the severity of the heart failure and any other associated lesions
Heart
The apical impulse is sustained and nondisplaced in patients without significant systolic LV
dysfunction but with LVH. A presystolic S4 may be felt. Later in the course of disease, when
significant systolic LV dysfunction supervenes, the apical impulse is displaced laterally, owing to
LV dilatation. In the right ventricle, a lift is present late in the course of heart failure if significant
pulmonary hypertension develops.
S1 is normal in intensity and character. S2 at the right upper sternal border is loud because of an
accentuated aortic component (A2); it can have a reverse or paradoxical split due either to
increased afterload or to associated left bundle-branch block (LBBB). S4 is frequently palpable
and audible, implying the presence of a stiffened, noncompliant ventricle due to chronic pressure
overload and LVH. S3 is not typically present initially, but it is audible in the presence of heart
failure, either systolic or diastolic.
An early decrescendo diastolic murmur of aortic insufficiency may be heard along the midparasternal to left parasternal area, especially in the presence of acutely elevated BP, frequently
disappearing once the BP is better controlled. In addition, an early systolic to midsystolic
murmur of aortic sclerosis is commonly audible. A holosystolic murmur of mitral regurgitation
may be present in patients with advanced heart failure and a dilated mitral annulus.
Lungs
Findings upon chest examination may be normal or may include signs of pulmonary congestion,
such as rales, decreased breath sounds, and dullness to percussion due to pleural effusion.
Abdomen
The abdominal examination may reveal a renal artery bruit in patients with hypertension
secondary to renal artery stenosis, a pulsatile expansile mass of abdominal aortic aneurysm, and
hepatomegaly and ascites due to CHF.
Extremities
Ankle edema may be present in patients with advanced heart failure.
Central nervous system and ophthalmologic system
Central nervous system (CNS) examination findings are usually unremarkable unless the patient
has had previous cerebrovascular accidents with residual deficit. CNS changes may also be seen
in patients who present with hypertensive emergency.
Staging of Hypertension
Although hypertensive heart disease typically is not described in various stages, the disease
usually progresses in the following sequence:
Increased wall stress leads to LVH
Which leads to diastolic LV dysfunction
Which can be followed by systolic LV dysfunction
The risks of ventricular ectopy, ventricular arrhythmias, sudden cardiac death, and cardiovascular
mortality are increased in patients once LVH develops and are also increased in patients with
heart failure. Table 1, below, shows the division of BP and hypertension into stages.
Table 1. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint
National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure[12] (Open Table in a new window)
Category
Systolic BP,mm Hg
Optimal
< 120
< 80
Prehypertension
120-139
80-89
Stage I
140-159
Stage II
>160
Diastolic BP,mm Hg
90-99
>100
Laboratory Studies
Laboratory studies are helpful in establishing the etiology of hypertension, quantitating the
severity of target organ damage, and monitoring the adverse effects of therapy. The tests to be
ordered depend on clinical judgment regarding the etiology of hypertension.
Recommendations from the Seventh Report of the Joint National Committee (JNC7) on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure include carrying out
the following baseline laboratory workup before initiating treatment for hypertension[12] :
Electrocardiogram
Urinalysis
Blood glucose and hematocrit levels
Serum potassium, creatinine (or the corresponding estimated glomerular filtration rate
[GFR]), and calcium measurements
Lipid profile after a 9- to 12-hour fast - Includes high density lipoprotein (HDL)
cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides
Optional tests - Include measurement of urinary albumin excretion or albumin/creatinine
ratio
Evaluating the renal system
Blood urea nitrogen (BUN) and creatinine levels are elevated in patients with renal failure. Other
studies include the above-mentioned urinalysis, GFR, and urinary albumin excretion or
albumin/creatinine ratio measurements.
Evaluating the endocrine system
Hypokalemia is found in patients with primary hyperaldosteronism and in patients with
secondary hyperaldosteronism, Cushing disease, and Bartter syndrome. Hypokalemia is most
useful in leading to further diagnostic studies if the patient has not received diuretics.
Plasma renin activity is generally depressed and serum aldosterone level is elevated in patients
with primary hyperaldosteronism. Twenty-four – hour urinary catecholamine and metanephrine
levels are elevated in patients with pheochromocytoma.
Elevated 24-hour urinary free cortisol and failure to suppress an early morning serum cortisol
level after an overnight dexamethasone suppression test are observed in patients with Cushing
disease. Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in
patients with hyperthyroidism.
transthoracic Echocardiography
Transthoracic echocardiography (TTE) may be very useful for identifying features of
hypertensive heart disease. TTE is more sensitive and specific then electrocardiography for
diagnosing the presence of LVH (57% for mild and 98% for severe LVH). LVH is symmetrical,
whereas the hypertrophy of hypertrophic cardiomyopathy is asymmetrical. The definition of the
LVH based on echocardiography findings is somewhat controversial in the absence of any
criterion standards
Electrocardiography
LVH criteria
Various criteria, differing in sensitivity and specificity, have been used to diagnose LVH. Note
that the specificities and sensitivities of the different approaches are far less than those of
echocardiography. The frequency of LVH on ECG at the time of initial diagnosis varies from
10% to 100%; in one trial, for example, the frequency was 13%. The sensitivity of ECG for
diagnosing LVH is limited, approximately 30-57% in patients with severe LVH.
The Cornell criteria (most sensitive) are (1) R wave in aVL plus an S wave in V3 of greater than
2.8 mV in men and greater than 2mV in women. The Cornell and Cornell voltage duration
(Cornell voltage multiplied by QRS duration) criteria have a sensitivity as high as 95% and a
specificity as high as 50-60%. A Cornell voltage duration of greater than 2440mV/ms-1
particularly identifies the highest-risk patients.
The Sokolow-Lyon criteria are an S wave in V1 plus an R wave in V5 or V6 of greater than
3.5mV or an R wave in V5 or V6 of greater than 2.6mV. The sensitivity of these criteria is 25%,
with a specificity of close to 95%. The Gubner-Ungerleider criteria are an R wave in I plus an S
wave in III of greater than 2.5mV. Another set of LVH criteria, the Romhilt-Estes criteria, are
summarized in Table 2, below.
Table 2. Romhilt-Estes Criteria (A Point Score System*)
Voltage Criteria
Points
R wave or S wave in any limb lead >0.2mV or S wave in lead V1 or V2 or R wave in V5 or V6
>0.3mV
=3
LV strain (ST and T waves in direction opposite to QRS direction) without digitalis
=3
LV strain (ST and T waves in direction opposite to QRS direction) with digitalis
=1
LA enlargement (terminal negativity of P waves in V1 >0.1mV deep and 0.04 seconds wide)
=3
Left-axis deviation greater than -30°
=2
QRS duration greater than 0.09 seconds
=1
Intrinsicoid deflection in V5 or V6 >0.05 seconds
=1
* Probable LVH is 4 points; definite LVH is 5 points. The sensitivity of these criteria is 50%,
with a specificity of close to 95%.
Blood Pressure Goals and Consultations
The medical care of patients with hypertensive heart disease falls under 2 categories—treatment
of the elevated BP and prevention and treatment of hypertensive heart disease. According to JNC
7, BP goals should be as follows[12]
Less than 140/90mm Hg in patients with uncomplicated hypertension
Less than 130/85mm Hg in patients with diabetes and those with renal disease with less
than 1g/24-hour proteinuria
Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-
Lifestyle Modifications
Emerging data support a target BP goal of less than 150/80mm Hg in patients older than 80 years
as a means of reducing the risk of congestive heart failure by 64%.[14] Various treatment
strategies include the following:
Dietary modifications
Regular aerobic exercise
Weight loss[15]
Pharmacotherapy directed toward hypertension, heart failure secondary to diastolic and
systolic LV dysfunction, coronary artery disease, and arrhythmias
Dietary modifications
Studies have shown that diet and a healthy lifestyle alone or in combination with medical
treatment can lower BP and decrease the symptoms of heart failure, as well as reverse LVH. A
heart-healthy diet is part of the secondary prophylaxis in patients with coronary artery disease
and of the primary prophylaxis in patients at high risk for this disease. Specific dietary
recommendations include a diet low in sodium, high in potassium (in patients with normal renal
function), rich in fresh fruits and vegetables, low in cholesterol, and low in alcohol consumption.
[16, 17, 18]
In a large cohort study of women, the following 6 modifiable lifestyle and dietary factors for
lowering the risk of hypertension were identified[19] :
A body mass index (BMI) below 25kg/m2
Vigorous exercise for a daily mean period of 30 minutes
A high score on the Dietary Approaches to Stop Hypertension (DASH) diet
Modest alcohol intake (up to 10g/day)
Nonnarcotic analgesic use less than once weekly
Intake of 400mcg/day or more of supplemental folic acid
A low-sodium diet, alone or in combination with pharmacotherapy, has been shown by numerous
studies to reduce BP in patients with hypertension, with a more prominent response in a subset of
patients with hypertension—mainly black individuals—with low renin levels. Restriction of
sodium in these patients does not lead to compensatory stimulation of the renin-angiotensin
system and thus has a potent antihypertensive effect. Data also indicate that sodium reduction,
previously shown to lower BP, may also reduce the long-term risk of cardiovascular events. The
recommended daily sodium intake is 50-100mmol, equivalent to 3-6g of salt per day, which
leads to an average 2-8mm Hg reduction in BP.[20]
In various epidemiologic studies, a high-potassium diet has been associated with lowering of BP.
The mechanism of this action is not clear. Intravenous infusion of potassium has been shown to
cause vasodilatation, which is believed to be mediated by nitric oxide in the vascular wall. Fresh
fruits and vegetables rich in potassium, such as bananas, oranges, avocados, and tomatoes,
should be recommended for patients with normal renal function.
The DASH diet has been shown to significantly lower the BP (8-14mm Hg) in patients with
hypertension regardless of whether or not they maintain a constant sodium content in their diet.
The DASH diet is not only rich in important nutrients and fiber but also includes foods that
contain far more potassium, calcium, and magnesium than are found in the average American
diet. This diet should be advised in patients with hypertension.[21, 22, 23, 24, 25]
Heavy alcohol consumption has been associated with high BP and an increase in LV mass.[26]
Moderation in alcohol consumption is advised; no more than 1-2 drinks daily is recommended.
[27]
Sinha et al concluded that high intakes of red or processed meat were associated with modest
increases in total mortality, cancer mortality, and cardiovascular disease mortality.[28] The
baseline population was a cohort of one-half million people aged 50-71 years from the National
Institutes of Health (NIH)-AARP (formerly known as the American Association of Retired
Persons) Diet and Health Study.[28]
Exercise
Regular dynamic isotonic (aerobic) exercise, such as walking, running, swimming, or cycling,
has been shown to decrease BP and improve cardiovascular well-being.[29] It also has additional
favorable cardiovascular effects, including improved endothelial function, peripheral
vasodilatation, reduced resting heart rate, improved heart rate variability, and reduced plasma
levels of catecholamines.
Regular aerobic exercise sessions of at least 30 minutes for most days of the week can produce
an average reduction in BP of 4-9mm Hg. Isometric and strenuous exercise should be avoided.
Weight reduction
Studies have shown that weight reduction is one of the most effective ways to reduce BP. A 520mm Hg BP reduction occurs with each 10kg of weight loss.[30] Gradual weight reduction
(1kg weekly) should be advised. Pharmacologic interventions to reduce weight should be used
with great caution, because diet pills, especially those available over the counter, frequently
contain sympathomimetics. These agents can raise BP, worsen angina or symptoms of heart
failure, and exacerbate tendencies for cardiac arrhythmias. Medications that should be avoided
include nonsteroid anti-inflammatory drugs (NSAIDs), sympathomimetics, and monoamine
oxidase inhibitors (MAOIs), as these agents can elevate BP or interfere with antihypertensive
therapy.hour proteinuria
Treatment of left ventricular hypertrophy
LVH, a marker of increased risk of cardiovascular morbidity and mortality, should be treated
aggressively because patients with LVH represent the subgroup of patients at the highest risk for
cardiovascular events and mortality. Whether regression in LVH leads to improvement in
cardiovascular mortality and morbidity rates is not clear, although limited data support this
hypothesis. Data also indicate that regression of electrocardiographic LVH is associated with less
hospitalization for heart failure in hypertensive patients.[32]
Medications for the treatment of hypertension have been shown to reduce LVH. Limited metaanalysis data suggest a slight advantage to ACE inhibitors.
Treatment of left ventricular diastolic dysfunction
Certain classes of antihypertensives—ACE inhibitors, beta blockers, and nondihydropyridine
calcium channel blockers—have been shown (although not consistently) to improve
echocardiographic parameters in symptomatic and asymptomatic diastolic dysfunction and the
symptomatology of heart failure. Candesartan, an ARB, has been shown to decrease
hospitalization in patients with diastolic heart failure.[34]
Use diuretics and nitrates with caution in patients with heart failure due to diastolic dysfunction.
These drugs may cause severe hypotension by inappropriately decreasing the preload, which is
required for adequate LV filling pressures. If diuretics are indicated, delicate titration is
necessary. Hydralazine has been shown to cause severe hypotension in patients with heart failure
due to diastolic dysfunction.
By increasing the intracellular calcium level, digoxin can worsen LV stiffness. However, a large,
randomized trial has not shown any increase in mortality rate.
Treatment of left ventricular systolic dysfunction
Diuretics (predominantly loop diuretics) are used in the treatment of LV systolic dysfunction.
Low-dose spironolactone has been shown to decrease the rates of morbidity and mortality in
patients in NYHA class III or IV heart failure who are already taking ACE inhibitors. This agent
is also recommended for use in post-myocardial infarction patients with diabetes mellitus or who
have an LV ejection fraction of less than 40%.[35]
ACE inhibitors are used for preload and afterload reduction and the prevention of pulmonary or
systemic congestion. These drugs have been shown to decrease morbidity and mortality rates in
patients with heart failure due to systolic dysfunction. The aim should be to use the target dose or
the maximum tolerable doses. ACE inhibitors are also indicated in patients with asymptomatic
LV dilatation and dysfunction.
Beta blockers (cardioselective or mixed alpha and beta), such as carvedilol, metoprolol XL, and
bisoprolol, have been shown to improve LV function and decrease rates of mortality and
morbidity from heart failure. Trials have also shown improvement in outcomes for patients in
NYHA class IV heart failure with carvedilol administration. These drugs should be started when
the patient has no signs of fluid overload and is in compensated heart failure. Therapy should be
initiated with low doses, increasing the dose of the beta blocker very slowly and closely
monitoring the patient for signs of worsening heart failure.
Treatment of cardiac arrhythmias
The treatment of these conditions depends upon the specific arrhythmia and the underlying LV
function, Anticoagulation should be considered in patients with atrial fibrillation. In addition,
treat anxiety, stress, sleep apnea, and other contributing or precipitating factors.
Cardiovascular effects of hypertension
Uncontrolled and prolonged elevation of BP can lead to a variety of changes in the myocardial
structure, coronary vasculature, and conduction system of the heart. These changes in turn can
lead to the development of left ventricular hypertrophy (LVH), coronary artery disease (CAD),
various conduction system diseases, and systolic and diastolic dysfunction of the myocardium,
complications that manifest clinically as angina or myocardial infarction, cardiac arrhythmias
(especially atrial fibrillation), and congestive heart failure (CHF).
Thus, hypertensive heart disease is a term applied generally to heart diseases, such as coronary
artery disease, cardiac arrhythmias, and CHF, that are caused by the direct or indirect effects of
elevated BP. Although these diseases generally develop in response to chronically elevated BP,
marked and acute elevation of BP can lead to accentuation of an underlying predisposition to any
of the symptoms traditionally associated with chronic hypertension.
Etiology
The etiology of hypertensive heart disease is a complex interplay of various hemodynamic,
structural, neuroendocrine, cellular, and molecular factors. These factors play integral roles in the
development of hypertension and its complications; however, elevated BP it self can modulate
these factors.
Obesity has been linked to hypertension and LVH in various epidemiologic studies, with as
many as 50% of obese patients having some degree of hypertension and as many as 60-70% of
patients with hypertension being obese.
Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly, by
increased afterload, and indirectly, by associated neurohormonal and vascular changes. Elevated
24-hour ambulatory BP and nocturnal BP have been demonstrated to be more closely related to
various cardiac pathologies, especially in black persons. The pathophysiologies of the various
cardiac effects of hypertension differ and are described in this section.
Left ventricular hypertrophy
LVH, defined as an increase in the mass of the left ventricle, is caused by the response of
myocytes to various stimuli accompanying elevated BP. Myocyte hypertrophy can occur as a
compensatory response to increased afterload. Mechanical and neurohormonal stimuli
accompanying hypertension can lead to activation of myocardial cell growth, gene expression (of
which some occurs primarily in fetal cardiomyocytes), and, thus, to LVH.
In addition, activation of the renin-angiotensin system, through the action of angiotensin II on
angiotensin I receptors, leads to growth of interstitium and cell matrix components. In summary,
the development of LVH is characterized by myocyte hypertrophy and by an imbalance between
the myocytes and the interstitium of the myocardial skeletal structure.
Various patterns of LVH have been described, including concentric remodeling, concentric LVH,
and eccentric LVH. Concentric LVH is an increase in LV thickness and LV mass with increased
LV diastolic pressure and volume, commonly observed in persons with hypertension; this is a
marker of poor prognosis in these patients. Compare concentric LVH with eccentric LVH, in
which LV thickness is increased not uniformly but at certain sites, such as the septum.
Although the development of LVH initially plays a protective role in response to increased wall
stress to maintain adequate cardiac output, it later leads to the development of diastolic and,
ultimately, systolic myocardial dysfunction.
Left atrial abnormalities
Frequently underappreciated, structural and functional changes of the left atrium are very
common in patients with hypertension. The increased afterload imposed on the LA by the
elevated LV end-diastolic pressure secondary to increased BP leads to impairment of the left
atrium and left atrial (LA) appendage function, plus increased LA size and thickness.
Increased LA size accompanying hypertension in the absence of valvular heart disease or systolic
dysfunction usually implies chronicity of hypertension and may correlate with the severity of LV
diastolic dysfunction.
In addition to LA structural changes, these patients are predisposed to atrial fibrillation. Atrial
fibrillation, with loss of atrial contribution in the presence of diastolic dysfunction, may
precipitate overt heart failure.
Valvular disease
Although valvular disease does not cause hypertensive heart disease, chronic and severe
hypertension can cause aortic root dilatation, leading to significant aortic insufficiency. Some
degree of hemodynamically insignificant aortic insufficiency is often found in patients with
uncontrolled hypertension. An acute rise in BP may accentuate the degree of aortic insufficiency,
with return to baseline when the BP is better controlled. In addition to causing aortic
regurgitation, hypertension is also thought to accelerate the process of aortic sclerosis and cause
mitral regurgitation.
Heart failure
Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart
failure develops, the dysfunctioning left ventricle is unable to generate the high BP, thus
obscuring the heart failure's etiology. The prevalence of asymptomatic diastolic dysfunction in
patients with hypertension and without LVH may be as high as 33%. Chronically elevated
afterload and the resulting LVH can adversely affect the active early relaxation phase and the late
compliance phase of ventricular diastole.
Diastolic dysfunction
Diastolic dysfunction is common in persons with hypertension. It is often, but not invariably,
accompanied by LVH. In addition to elevated afterload, other factors that may contribute to the
development of diastolic dysfunction include coexistent coronary artery disease, aging, systolic
dysfunction, and structural abnormalities such as fibrosis and LVH. Asymptomatic systolic
dysfunction usually follows.
Systolic dysfunction
Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the
face of elevated BP, and the LV cavity begins to dilate to maintain cardiac output. As the disease
enters the end stage, LV systolic function decreases further. This leads to further increases in
activation of the neurohormonal and renin-angiotensin systems, leading to increases in salt and
water retention and increased peripheral vasoconstriction. Eventually, the already compromised
LV is overwhelmed, and the patient progresses to the stage of symptomatic systolic dysfunction.
Decompensation
Apoptosis, or programmed cell death, stimulated by myocyte hypertrophy and the imbalance
between its stimulants and inhibitors, is considered to play an important part in the transition
from compensated to decompensated stage. The patient may become symptomatic during the
asymptomatic stages of the LV systolic or diastolic dysfunction, owing to changes in afterload
conditions or to the presence of other insults to the myocardium (eg, ischemia, infarction). A
sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV
ejection fraction.
Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds
rapid deterioration in clinical status and a markedly increased risk of death. In addition to LV
dysfunction, right ventricular (RV) thickening and diastolic dysfunction also develop as results of
septal thickening and LV dysfunction.
Myocardial ischemia
Patients with angina have a high prevalence of hypertension. Hypertension is an established risk
factor for the development of coronary artery disease, almost doubling the risk. The development
of ischemia in patients with hypertension is multifactorial.
Importantly, in patients with hypertension, angina can occur in the absence of epicardial
coronary artery disease. The reason for this is 2-fold. Increased afterload secondary to
hypertension leads to an increase in LV wall tension and transmural pressure, compromising
coronary blood flow during diastole. In addition, the microvasculature beyond the epicardial
coronary arteries has been shown to be dysfunctional in patients with hypertension, and it may be
unable to compensate for increased metabolic and oxygen demand.
The development and progression of arteriosclerosis, the hallmark of coronary artery disease, is
exacerbated in arteries subjected to chronically elevated BP. Shear stress associated with
hypertension and the resulting endothelial dysfunction cause impairment in the synthesis and
release of the potent vasodilator nitric oxide. A decreased nitric oxide level promotes the
development and acceleration of arteriosclerosis and plaque formation. Morphologic features of
the plaque are identical to those observed in patients without hypertension.
Cardiac arrhythmias
Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation,
premature ventricular contractions (PVCs), and ventricular tachycardia (VT).[7] The risk of
sudden cardiac death is increased.[8] Various mechanisms thought to play a part in the
pathogenesis of arrhythmias include altered cellular structure and metabolism, inhomogeneity of
the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these
may lead to an increased risk of ventricular tachyarrhythmias.
Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in
patients with hypertension.[9] In fact, elevated BP is the most common cause of atrial fibrillation
in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had
hypertension. Although the exact etiology is not known, LA structural abnormalities, associated
coronary artery disease, and LVH have been suggested as possible contributing factors. The
development of atrial fibrillation can cause decompensation of systolic and, more importantly,
diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of
thromboembolic complications, most notably stroke.
Premature ventricular contractions, ventricular arrhythmias, and sudden cardiac death are
observed more often in patients with LVH than in those without LVH. The etiology of these
arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis.
Physical Examination
Physical signs of hypertensive heart disease depend on the predominant cardiac abnormality and
the duration and severity of the hypertensive heart disease. Findings from the physical
examination may be entirely normal in the very early stages of the disease, or the patient may
have classic signs upon examination.
Pulses
The arterial pulses are normal in the early stages of hypertensive heart disease. The cardiac
rhythm is regular if the patient is in sinus rhythm; it is irregularly irregular if the patient is in
atrial fibrillation. The heart rate is as follows:
Normal in patients in sinus rhythm
Not normal in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial fibrillation and a
rapid ventricular response
The pulse volume is usually normal, but it is decreased in patients with LV dysfunction.
Additional findings may include radial-femoral delay if the etiology of hypertension is
coarctation of the aorta
Blood pressure
Systolic and/or diastolic BP is elevated (>140/90mm Hg). Mean BP and pulse pressure are also
elevated generally. The BP in the upper extremities may be higher than that in the lower
extremities in patients with coarctation of the aorta. BP may be normal at the time of evaluation
if the patient is on adequate antihypertensive medications or if the patient has advanced LV
dysfunction and the LV cannot generate enough stroke volume and cardiac output to produce an
elevated BP.
Veins
In patients with heart failure, the jugular veins may be distended. The predominant waves depend
on the severity of the heart failure and any other associated lesions
Heart
The apical impulse is sustained and nondisplaced in patients without significant systolic LV
dysfunction but with LVH. A presystolic S4 may be felt. Later in the course of disease, when
significant systolic LV dysfunction supervenes, the apical impulse is displaced laterally, owing to
LV dilatation. In the right ventricle, a lift is present late in the course of heart failure if significant
pulmonary hypertension develops.
S1 is normal in intensity and character. S2 at the right upper sternal border is loud because of an
accentuated aortic component (A2); it can have a reverse or paradoxical split due either to
increased afterload or to associated left bundle-branch block (LBBB). S4 is frequently palpable
and audible, implying the presence of a stiffened, noncompliant ventricle due to chronic pressure
overload and LVH. S3 is not typically present initially, but it is audible in the presence of heart
failure, either systolic or diastolic.
An early decrescendo diastolic murmur of aortic insufficiency may be heard along the midparasternal to left parasternal area, especially in the presence of acutely elevated BP, frequently
disappearing once the BP is better controlled. In addition, an early systolic to midsystolic
murmur of aortic sclerosis is commonly audible. A holosystolic murmur of mitral regurgitation
may be present in patients with advanced heart failure and a dilated mitral annulus.
Lungs
Findings upon chest examination may be normal or may include signs of pulmonary congestion,
such as rales, decreased breath sounds, and dullness to percussion due to pleural effusion.
Abdomen
The abdominal examination may reveal a renal artery bruit in patients with hypertension
secondary to renal artery stenosis, a pulsatile expansile mass of abdominal aortic aneurysm, and
hepatomegaly and ascites due to CHF.
Extremities
Ankle edema may be present in patients with advanced heart failure.
Central nervous system and ophthalmologic system
Central nervous system (CNS) examination findings are usually unremarkable unless the patient
has had previous cerebrovascular accidents with residual deficit. CNS changes may also be seen
in patients who present with hypertensive emergency.
Staging of Hypertension
Although hypertensive heart disease typically is not described in various stages, the disease
usually progresses in the following sequence:
Increased wall stress leads to LVH
Which leads to diastolic LV dysfunction
Which can be followed by systolic LV dysfunction
The risks of ventricular ectopy, ventricular arrhythmias, sudden cardiac death, and cardiovascular
mortality are increased in patients once LVH develops and are also increased in patients with
heart failure. Table 1, below, shows the division of BP and hypertension into stages.
Table 1. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint
National Committee (JNC7) on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure[12] (Open Table in a new window)
Category
Systolic BP,mm Hg
Optimal
< 120
< 80
Prehypertension
120-139
80-89
Stage I
140-159
Stage II
>160
Diastolic BP,mm Hg
90-99
>100
Laboratory Studies
Laboratory studies are helpful in establishing the etiology of hypertension, quantitating the
severity of target organ damage, and monitoring the adverse effects of therapy. The tests to be
ordered depend on clinical judgment regarding the etiology of hypertension.
Recommendations from the Seventh Report of the Joint National Committee (JNC7) on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure include carrying out
the following baseline laboratory workup before initiating treatment for hypertension[12] :
Electrocardiogram
Urinalysis
Blood glucose and hematocrit levels
Serum potassium, creatinine (or the corresponding estimated glomerular filtration rate
[GFR]), and calcium measurements
Lipid profile after a 9- to 12-hour fast - Includes high density lipoprotein (HDL)
cholesterol, low-density lipoprotein (LDL) cholesterol, and triglycerides
Optional tests - Include measurement of urinary albumin excretion or albumin/creatinine
ratio
Evaluating the renal system
Blood urea nitrogen (BUN) and creatinine levels are elevated in patients with renal failure. Other
studies include the above-mentioned urinalysis, GFR, and urinary albumin excretion or
albumin/creatinine ratio measurements.
Evaluating the endocrine system
Hypokalemia is found in patients with primary hyperaldosteronism and in patients with
secondary hyperaldosteronism, Cushing disease, and Bartter syndrome. Hypokalemia is most
useful in leading to further diagnostic studies if the patient has not received diuretics.
Plasma renin activity is generally depressed and serum aldosterone level is elevated in patients
with primary hyperaldosteronism. Twenty-four – hour urinary catecholamine and metanephrine
levels are elevated in patients with pheochromocytoma.
Elevated 24-hour urinary free cortisol and failure to suppress an early morning serum cortisol
level after an overnight dexamethasone suppression test are observed in patients with Cushing
disease. Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in
patients with hyperthyroidism.
transthoracic Echocardiography
Transthoracic echocardiography (TTE) may be very useful for identifying features of
hypertensive heart disease. TTE is more sensitive and specific then electrocardiography for
diagnosing the presence of LVH (57% for mild and 98% for severe LVH). LVH is symmetrical,
whereas the hypertrophy of hypertrophic cardiomyopathy is asymmetrical. The definition of the
LVH based on echocardiography findings is somewhat controversial in the absence of any
criterion standards
Electrocardiography
LVH criteria
Various criteria, differing in sensitivity and specificity, have been used to diagnose LVH. Note
that the specificities and sensitivities of the different approaches are far less than those of
echocardiography. The frequency of LVH on ECG at the time of initial diagnosis varies from
10% to 100%; in one trial, for example, the frequency was 13%. The sensitivity of ECG for
diagnosing LVH is limited, approximately 30-57% in patients with severe LVH.
The Cornell criteria (most sensitive) are (1) R wave in aVL plus an S wave in V3 of greater than
2.8 mV in men and greater than 2mV in women. The Cornell and Cornell voltage duration
(Cornell voltage multiplied by QRS duration) criteria have a sensitivity as high as 95% and a
specificity as high as 50-60%. A Cornell voltage duration of greater than 2440mV/ms-1
particularly identifies the highest-risk patients.
The Sokolow-Lyon criteria are an S wave in V1 plus an R wave in V5 or V6 of greater than
3.5mV or an R wave in V5 or V6 of greater than 2.6mV. The sensitivity of these criteria is 25%,
with a specificity of close to 95%. The Gubner-Ungerleider criteria are an R wave in I plus an S
wave in III of greater than 2.5mV. Another set of LVH criteria, the Romhilt-Estes criteria, are
summarized in Table 2, below.
Table 2. Romhilt-Estes Criteria (A Point Score System*)
Voltage Criteria
Points
R wave or S wave in any limb lead >0.2mV or S wave in lead V1 or V2 or R wave in V5 or V6
>0.3mV
=3
LV strain (ST and T waves in direction opposite to QRS direction) without digitalis
=3
LV strain (ST and T waves in direction opposite to QRS direction) with digitalis
=1
LA enlargement (terminal negativity of P waves in V1 >0.1mV deep and 0.04 seconds wide)
=3
Left-axis deviation greater than -30°
=2
QRS duration greater than 0.09 seconds
=1
Intrinsicoid deflection in V5 or V6 >0.05 seconds
=1
* Probable LVH is 4 points; definite LVH is 5 points. The sensitivity of these criteria is 50%,
with a specificity of close to 95%.
Blood Pressure Goals and Consultations
The medical care of patients with hypertensive heart disease falls under 2 categories—treatment
of the elevated BP and prevention and treatment of hypertensive heart disease. According to JNC
7, BP goals should be as follows[12]
Less than 140/90mm Hg in patients with uncomplicated hypertension
Less than 130/85mm Hg in patients with diabetes and those with renal disease with less
than 1g/24-hour proteinuria
Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-
Lifestyle Modifications
Emerging data support a target BP goal of less than 150/80mm Hg in patients older than 80 years
as a means of reducing the risk of congestive heart failure by 64%.[14] Various treatment
strategies include the following:
Dietary modifications
Regular aerobic exercise
Weight loss[15]
Pharmacotherapy directed toward hypertension, heart failure secondary to diastolic and
systolic LV dysfunction, coronary artery disease, and arrhythmias
Dietary modifications
Studies have shown that diet and a healthy lifestyle alone or in combination with medical
treatment can lower BP and decrease the symptoms of heart failure, as well as reverse LVH. A
heart-healthy diet is part of the secondary prophylaxis in patients with coronary artery disease
and of the primary prophylaxis in patients at high risk for this disease. Specific dietary
recommendations include a diet low in sodium, high in potassium (in patients with normal renal
function), rich in fresh fruits and vegetables, low in cholesterol, and low in alcohol consumption.
[16, 17, 18]
In a large cohort study of women, the following 6 modifiable lifestyle and dietary factors for
lowering the risk of hypertension were identified[19] :
A body mass index (BMI) below 25kg/m2
Vigorous exercise for a daily mean period of 30 minutes
A high score on the Dietary Approaches to Stop Hypertension (DASH) diet
Modest alcohol intake (up to 10g/day)
Nonnarcotic analgesic use less than once weekly
Intake of 400mcg/day or more of supplemental folic acid
A low-sodium diet, alone or in combination with pharmacotherapy, has been shown by numerous
studies to reduce BP in patients with hypertension, with a more prominent response in a subset of
patients with hypertension—mainly black individuals—with low renin levels. Restriction of
sodium in these patients does not lead to compensatory stimulation of the renin-angiotensin
system and thus has a potent antihypertensive effect. Data also indicate that sodium reduction,
previously shown to lower BP, may also reduce the long-term risk of cardiovascular events. The
recommended daily sodium intake is 50-100mmol, equivalent to 3-6g of salt per day, which
leads to an average 2-8mm Hg reduction in BP.[20]
In various epidemiologic studies, a high-potassium diet has been associated with lowering of BP.
The mechanism of this action is not clear. Intravenous infusion of potassium has been shown to
cause vasodilatation, which is believed to be mediated by nitric oxide in the vascular wall. Fresh
fruits and vegetables rich in potassium, such as bananas, oranges, avocados, and tomatoes,
should be recommended for patients with normal renal function.
The DASH diet has been shown to significantly lower the BP (8-14mm Hg) in patients with
hypertension regardless of whether or not they maintain a constant sodium content in their diet.
The DASH diet is not only rich in important nutrients and fiber but also includes foods that
contain far more potassium, calcium, and magnesium than are found in the average American
diet. This diet should be advised in patients with hypertension.[21, 22, 23, 24, 25]
Heavy alcohol consumption has been associated with high BP and an increase in LV mass.[26]
Moderation in alcohol consumption is advised; no more than 1-2 drinks daily is recommended.
[27]
Sinha et al concluded that high intakes of red or processed meat were associated with modest
increases in total mortality, cancer mortality, and cardiovascular disease mortality.[28] The
baseline population was a cohort of one-half million people aged 50-71 years from the National
Institutes of Health (NIH)-AARP (formerly known as the American Association of Retired
Persons) Diet and Health Study.[28]
Exercise
Regular dynamic isotonic (aerobic) exercise, such as walking, running, swimming, or cycling,
has been shown to decrease BP and improve cardiovascular well-being.[29] It also has additional
favorable cardiovascular effects, including improved endothelial function, peripheral
vasodilatation, reduced resting heart rate, improved heart rate variability, and reduced plasma
levels of catecholamines.
Regular aerobic exercise sessions of at least 30 minutes for most days of the week can produce
an average reduction in BP of 4-9mm Hg. Isometric and strenuous exercise should be avoided.
Weight reduction
Studies have shown that weight reduction is one of the most effective ways to reduce BP. A 520mm Hg BP reduction occurs with each 10kg of weight loss.[30] Gradual weight reduction
(1kg weekly) should be advised. Pharmacologic interventions to reduce weight should be used
with great caution, because diet pills, especially those available over the counter, frequently
contain sympathomimetics. These agents can raise BP, worsen angina or symptoms of heart
failure, and exacerbate tendencies for cardiac arrhythmias. Medications that should be avoided
include nonsteroid anti-inflammatory drugs (NSAIDs), sympathomimetics, and monoamine
oxidase inhibitors (MAOIs), as these agents can elevate BP or interfere with antihypertensive
therapy.hour proteinuria
Treatment of left ventricular hypertrophy
LVH, a marker of increased risk of cardiovascular morbidity and mortality, should be treated
aggressively because patients with LVH represent the subgroup of patients at the highest risk for
cardiovascular events and mortality. Whether regression in LVH leads to improvement in
cardiovascular mortality and morbidity rates is not clear, although limited data support this
hypothesis. Data also indicate that regression of electrocardiographic LVH is associated with less
hospitalization for heart failure in hypertensive patients.[32]
Medications for the treatment of hypertension have been shown to reduce LVH. Limited metaanalysis data suggest a slight advantage to ACE inhibitors.
Treatment of left ventricular diastolic dysfunction
Certain classes of antihypertensives—ACE inhibitors, beta blockers, and nondihydropyridine
calcium channel blockers—have been shown (although not consistently) to improve
echocardiographic parameters in symptomatic and asymptomatic diastolic dysfunction and the
symptomatology of heart failure. Candesartan, an ARB, has been shown to decrease
hospitalization in patients with diastolic heart failure.[34]
Use diuretics and nitrates with caution in patients with heart failure due to diastolic dysfunction.
These drugs may cause severe hypotension by inappropriately decreasing the preload, which is
required for adequate LV filling pressures. If diuretics are indicated, delicate titration is
necessary. Hydralazine has been shown to cause severe hypotension in patients with heart failure
due to diastolic dysfunction.
By increasing the intracellular calcium level, digoxin can worsen LV stiffness. However, a large,
randomized trial has not shown any increase in mortality rate.
Treatment of left ventricular systolic dysfunction
Diuretics (predominantly loop diuretics) are used in the treatment of LV systolic dysfunction.
Low-dose spironolactone has been shown to decrease the rates of morbidity and mortality in
patients in NYHA class III or IV heart failure who are already taking ACE inhibitors. This agent
is also recommended for use in post-myocardial infarction patients with diabetes mellitus or who
have an LV ejection fraction of less than 40%.[35]
ACE inhibitors are used for preload and afterload reduction and the prevention of pulmonary or
systemic congestion. These drugs have been shown to decrease morbidity and mortality rates in
patients with heart failure due to systolic dysfunction. The aim should be to use the target dose or
the maximum tolerable doses. ACE inhibitors are also indicated in patients with asymptomatic
LV dilatation and dysfunction.
Beta blockers (cardioselective or mixed alpha and beta), such as carvedilol, metoprolol XL, and
bisoprolol, have been shown to improve LV function and decrease rates of mortality and
morbidity from heart failure. Trials have also shown improvement in outcomes for patients in
NYHA class IV heart failure with carvedilol administration. These drugs should be started when
the patient has no signs of fluid overload and is in compensated heart failure. Therapy should be
initiated with low doses, increasing the dose of the beta blocker very slowly and closely
monitoring the patient for signs of worsening heart failure.
Treatment of cardiac arrhythmias
The treatment of these conditions depends upon the specific arrhythmia and the underlying LV
function, Anticoagulation should be considered in patients with atrial fibrillation. In addition,
treat anxiety, stress, sleep apnea, and other contributing or precipitating factors.
