Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:

"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".

(HR. Muslim, Ahmad dan Hakim).

Kamis, 24 Desember 2009

Hypertensive Heart Disease


Uncontrolled and prolonged elevation of blood pressure (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, various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, which 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 LVH, coronary artery disease, cardiac arrhythmias, and CHF, that are caused by 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 also lead to accentuation of an underlying predisposition to any of the symptoms traditionally associated with chronic hypertension.

The pathophysiology of hypertensive heart disease is a complex interplay of various hemodynamic, structural, neuroendocrine, cellular, and molecular factors. On the one hand, these factors play integral roles in the development of hypertension and its complications; on the other hand, elevated BP itself can modulate these factors. 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 African Americans. The pathophysiologies of the various cardiac effects of hypertension differ and are described in this section.

Left ventricular hypertrophy

Of patients with hypertension, 15-20% develops LVH. The risk of LVH is increased 2-fold by associated obesity. The prevalence of LVH based on electrocardiogram (ECG) findings, which are not a sensitive marker at the time of diagnosis of hypertension, is variable.1,2 Studies have shown a direct relationship between the level and duration of elevated BP and LVH.

LVH, defined as an increase in the mass of the left ventricle (LV), 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 and which is a marker of poor prognosis in these patients. Compare this with eccentric LVH, in which LV thickness is increased not uniformly but at certain sites, such as the septum. While the development of LVH initially plays a protective role in response to increased wall stress to maintain adequate cardiac output, later it leads to the development of diastolic and, ultimately, systolic myocardial dysfunction.

Left atrial abnormalities

Frequently underappreciated, structural and functional changes of the left atrium (LA) 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 LA and 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 these 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 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

Heart failure is a common complication of chronically elevated BP. Hypertension as a cause of CHF is frequently underrecognized, partly because at the time heart failure develops, the dysfunctioning LV is unable to generate the high BP, thus obscuring the etiology of the heart failure. The prevalence of asymptomatic diastolic dysfunction in patients with hypertension and without LVH may be as high as 33%. Chronically elevated afterload and resulting LVH can adversely affect both the active early relaxation phase and late compliance phase of ventricular diastole.

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. Later in the course of disease, the LVH fails to compensate by increasing cardiac output in the face of elevated BP and the left ventricular 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 overwhelming the already compromised LV and progressing to the stage of symptomatic systolic dysfunction.

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.3 Generally, development of asymptomatic or symptomatic LV dilatation or dysfunction heralds rapid deterioration in clinical status and markedly increased risk of death. In addition to LV dysfunction, right ventricular 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 is 2-fold. Increased afterload secondary to hypertension leads to an increase in left ventricular 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 causes 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, and ventricular tachycardia.4

The risk of sudden cardiac death is increased.5 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.6 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, left atrial 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.

United States

The estimated prevalence of hypertension in 2005 was 35.3 million men and 38.3 million women.7

The exact frequency of LVH is unknown. The rate of LVH based on ECG findings is 2.9% for men and 1.5% for women. The rate based on echocardiography findings is 15-20%. Of patients without LVH, 33% have evidence of asymptomatic LV diastolic dysfunction.

According to the Framingham Study, hypertension accounts for about a quarter of heart failure cases.7 In the elderly population, as many as 68% of heart failure cases are attributed to hypertension. Community-based studies have demonstrated that hypertension may contribute to the development of heart failure in as many as 50-60% of patients. In patients with hypertension, the risk of heart failure is increased by 2-fold in men and by 3-fold in women.

Mortality and morbidity rates from hypertensive heart disease are higher than those of the general population and depend on the specific cardiac pathology.8 Data suggest that increases in mortality and morbidity rates are related more to the pulse pressure than the absolute systolic or diastolic BP levels, but all are important.

Left ventricular hypertrophy: The development of LVH is clearly related to an increase in the cardiovascular mortality rate. The increased risk of cardiovascular events with LVH depends on its type. Concentric LVH poses the greatest risk, as much as 30% over a 10-year period in one study, compared with 15% with eccentric remodeling and 9% without any LVH. The degree of LVH, as assessed by LV mass index (LVMI), is also related to the cardiovascular mortality rate, with a relative risk of 1.73 for men and 2.12 for women for each 50-g/m2 increase in the LVMI over a 4-year period. With LVH, the relative risk of mortality is increased 2-fold in patients with coronary artery disease and 4-fold in patients without coronary artery disease.9

Studies have also shown an increase in the risk of sudden cardiac death in patients with LVH.10 Regression of the LVMI has been demonstrated with several different antihypertensive medications. Although not proven, limited data suggest a reduction in LVH results in a reduction in cardiovascular events.
LV diastolic dysfunction: The prognosis of patients with diastolic dysfunction is poor and is affected by the presence of underlying coronary artery disease. In one study, survival rates at 3 months, 1 year, and 5 years in patients with heart failure due to diastolic dysfunction were 86%, 76%, and 46%, respectively. In another study, the 7-year cardiovascular mortality rate approached 50% in patients with heart failure due to diastolic dysfunction and concomitant coronary artery disease; some also had hypertension. Even in patients with asymptomatic diastolic dysfunction due to hypertension, risk of all cause mortality and cardiovascular events is significantly increased, particularly with an increase in the pulmonary artery wedge pressure. LV diastolic dysfunction, and the heart failure symptoms associated with it, has been shown to improve with treatment aimed at lowering BP and reducing LVH. Whether such treatment has any effect on the mortality rate is not clear.
LV systolic dysfunction: The mortality rate from heart failure due to systolic LV dysfunction is high and depends on the symptoms and New York Heart Association (NYHA) classification. The 5-year mortality rate for patients with heart failure due to systolic dysfunction approaches 20%, while the 2-year mortality rate in patients with NYHA class IV classification is as high as 50%. Mortality rates have decreased with use of ACE inhibitors and beta-blockers, which improve LV function.


In the United States, hypertension is more prevalent in African Americans than in Hispanic and non-Hispanic whites and it is increasing. From 1988-94 to 1999-2002, prevalence in this group increased from 35.8% to 41.4%. (Prevalence in whites is increasing as well but not as dramatically.)11 This difference is attributed to factors other than race because the prevalence of hypertension among African Americans and whites is the same in the United Kingdom and because hypertension is not very common on the African continent. In addition, hypertension is the most common etiology of heart failure in African Americans in the United States.

Systolic BP increases with age. This increase is more marked in men than in women until women reach menopause, when their BP rises more sharply and reaches levels higher than in men. The prevalence of hypertension is higher in men than in women younger than 55 years but is higher in women older than 55 years. The prevalence of hypertensive heart disease probably follows the same pattern.

BP increases with age, as does the prevalence of hypertensive heart disease, which is affected by the severity of BP increase.

Symptoms of hypertensive heart disease depend on the duration, severity, and type of disease. In addition, the patient may or may not be aware of the presence of hypertension, which is why hypertension has been named "the silent killer."

Left ventricular hypertrophy: Patients with LVH alone are totally asymptomatic unless the LVH leads to the development of diastolic dysfunction and heart failure.
Heart failure
Although symptomatic diastolic heart failure and systolic heart failure are indistinguishable, the clinical history may be quite revealing. In particular, individuals who abruptly develop severe symptoms of CHF and rapidly return to baseline with medical therapy are more likely to have isolated diastolic dysfunction.
Heart failure symptoms include the following:
Exertional and nonexertional dyspnea (NYHA classes I-IV)
Paroxysmal nocturnal dyspnea
Fatigue (more common in systolic dysfunction)
Ankle edema and weight gain
Abdominal pain secondary to congested, distended liver
Altered mentation in severe cases
Patients can present with acute pulmonary edema due to sudden decompensation in LV systolic or diastolic dysfunction caused by precipitating factors such as acute rise in BP, dietary indiscretion, or myocardial ischemia. Patients can develop cardiac arrhythmias, especially atrial fibrillation, or they can develop symptoms of heart failure insidiously over time.
Myocardial ischemia
Angina, a frequent complication of hypertensive heart disease, is also indistinguishable from other causes of myocardial ischemia.
Typical symptoms of angina include substernal chest pain lasting less than 15 minutes (versus >20 min in infarction). Pain is often described in the following ways:
Heaviness, pressure, squeezing
Radiating to neck, jaw, upper back, or left arm
Provoked by emotional or physical exertion
Relieved with rest or sublingual nitroglycerin
Patients also may present with atypical symptoms without chest pain, such as exertional dyspnea or excessive fatigue, commonly referred to as an angina equivalent. Female patients, in particular, are more likely to present with an atypical presentation
The patient may present with chronic stable angina or acute coronary syndrome, including myocardial infarction without ST-segment elevation and acute myocardial infarction with ST elevation. Ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography.
Acute coronary symptoms can be precipitated by a ruptured atherosclerotic plaque or by an acute and severe rise in BP leading to a sudden increase in transmural pressure without a change in stability of the plaque.
Cardiac arrhythmias: These can cause a variety of symptoms, including palpitations, near or total syncope, precipitation of angina, sudden cardiac death, and precipitation of heart failure, especially with atrial fibrillation in diastolic dysfunction.


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. In addition to generalized findings attributable directly to high BP, the physical examination may reveal clues to a potential etiology of hypertension, such as truncal obesity and striae in Cushing syndrome, renal artery bruit in renal artery stenosis, and abdominal mass in polycystic kidney disease.

Pulses: The arterial pulses are normal in the early stages of the disease.
Regular if the patient is in sinus rhythm
Irregularly irregular if the patient is in atrial fibrillation
Normal in patients in sinus rhythm and not in decompensated heart failure
Tachycardic in patients with heart failure and in patients with atrial fibrillation and a rapid ventricular response
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 (>140/90 mm Hg). Mean BP and pulse pressure generally are also elevated. 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 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, jugular veins may be distended; the predominant waves depend on the severity of the heart failure and any other associated lesions.
Apex: 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.
Right ventricle: A lift is present late in the course of heart failure if significant pulmonary hypertension develops.
Heart sounds: 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 frequently is palpable and audible, implying the presence of a stiffened, noncompliant ventricle due to chronic pressure overload and LVH. S3 typically is not present initially but is audible in the presence of heart failure, either systolic or diastolic.
Murmurs: An early decrescendo diastolic murmur of aortic insufficiency may be heard along the mid-to-left parasternal area, especially in the presence of acutely elevated BP, frequently disappearing once the BP is better controlled. In addition, an early to mid systolic murmur of aortic sclerosis is commonly audible. A holosystolic murmur of mitral regurgitation may be present in patients with advanced heart failure and 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: 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.
CNS and retina
CNS examination findings are usually unremarkable unless the patient has had previous cerebrovascular accidents with residual deficit.
Examination of the fundi may reveal evidence of hypertensive retinopathy, the severity of which depends on the duration and severity of hypertension, or earlier signs of hypertension such as arteriovenous nicking.
CNS changes may be seen in patients who present with hypertensive emergency.


The cause of hypertensive heart disease is chronically elevated BP. The causes of elevated BP are diverse. In adults, the following causes should be considered:

Essential hypertension accounts for 90% of cases of hypertension in adults.
Secondary causes of hypertension account for the remaining 10% of cases of chronically elevated BP. These include the following:
Renal causes
Renal artery stenosis
Polycystic kidney disease
Chronic renal failure
Intrarenal Vasculitis
Endocrine causes
Primary hyperaldosteronism
Cushing syndrome
Congenital adrenal hyperplasia
Hypothyroidism and hyperthyroidism
Exogenous hormone (eg, corticosteroids, estrogens), sympathomimetics (including cocaine), monoamine oxidase inhibitors (MAOIs), and tyramine-containing foods
Coarctation of aorta
Raised intracranial pressure
Sleep apnea
Isolated systolic hypertension - Can be observed in elderly people, due to increased stiffness of the vasculature
Isolated systolic hypertension - Can be observed in thyrotoxicosis, atrioventricular (AV) fistula, aortic regurgitation, beriberi, Paget disease, and patent ductus arteriosus (ie, due to increase cardiac output secondary to a hyperdynamic circulation)


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