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The cause of hypertensive heart disease is chronically elevated blood pressure (BP); however, the causes of elevated BP are diverse. 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. According to the Framingham Study, hypertension accounts for about one quarter of heart failure cases. 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.
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 LVH (seen in the images below), 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.
Two-dimensional echocardiogram (parasternal long axis view) from a 70-year-old woman showing concentric left ventricular hypertrophy and left atrial
Obesity has been linked to hypertension and LVH in various epidemiologic studies. and Heart Attack. 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. Gross specimen of the heart with concentric left ventricular hypertrophy. Elevated BP leads to adverse changes in cardiac structure and function in 2 ways: directly. Etiology The etiology of hypertensive heart disease is a complex interplay of various hemodynamic. by associated neurohormonal and vascular changes. cellular. by increased afterload. as well as High Blood Pressure. dietary modifications and the importance of regular exercise. Coronary Heart Disease. and indirectly. and avoiding medications and foods that can potentially elevate blood pressure should be emphasized. Elevated 24-hour ambulatory BP and nocturnal BP have been demonstrated to be more . elevated BP itself can modulate these factors. Differentials The following conditions should also be considered when evaluating hypertensive heart disease: Coronary artery atherosclerosis Hypertrophic cardiomyopathy Athlete's heart (with LVH) Congestive heart failure due to other etiologies Atrial fibrillation due to other etiologies Diastolic dysfunction due to other etiologies Sleep apnea Patient education It is important to educate patients about the nature of their disease and the risks associated with untreated hypertension.enlargement. These factors play integral roles in the development of hypertension and its complications. Chest Pain. and molecular factors. neuroendocrine. taking medications regularly. structural. see the Diabetes Center and the Cholesterol Center. In addition. however. weight loss. For patient education information. High Cholesterol.
the development of LVH is characterized by myocyte hypertrophy and by an imbalance between the myocytes and the interstitium of the myocardial skeletal structure.[3. commonly observed in persons with hypertension. LVH. Left ventricular hypertrophy Of patients with hypertension. systolic myocardial dysfunction. gene expression (of which some occurs primarily in fetal cardiomyocytes). The pathophysiologies of the various cardiac effects of hypertension differ and are described in this section. Concentric LVH is an increase in LV thickness and LV mass with increased LV diastolic pressure and volume.closely related to various cardiac pathologies. In addition. in which LV thickness is increased not uniformly but at certain sites. plus increased LA size and thickness. 4] Studies have shown a direct relationship between the level and duration of elevated BP and LVH. including concentric remodeling. Various patterns of LVH have been described. 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. this is a marker of poor prognosis in these patients. In summary. through the action of angiotensin II on angiotensin I receptors. Compare concentric LVH with eccentric LVH. is caused by the response of myocytes to various stimuli accompanying elevated BP. concentric LVH. Mechanical and neurohormonal stimuli accompanying hypertension can lead to activation of myocardial cell growth. 15-20% develop LVH. 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. The risk of LVH is increased 2-fold by associated obesity. is variable. Although the development of LVH initially plays a protective role in response to increased wall stress to maintain adequate cardiac output. to LVH. thus. The prevalence of LVH based on electrocardiogram (ECG) findings. it later leads to the development of diastolic and. such as the septum. Myocyte hypertrophy can occur as a compensatory response to increased afterload. ultimately. especially in black persons. leads to growth of interstitium and cell matrix components. . and eccentric LVH. findings from a prospective study (The Multiethnic Study of Atherosclerosis [MESA] trial) also indicate a higher risk of developing systemic hypertension among patients in the higher quartiles of the LV mass at baseline. Left atrial abnormalities Frequently underappreciated. Interestingly. which are not a sensitive marker at the time of diagnosis of hypertension. defined as an increase in the mass of the left ventricle. and. structural and functional changes of the left atrium are very common in patients with hypertension. activation of the renin-angiotensin system.
The prevalence of asymptomatic diastolic dysfunction in patients with hypertension and without LVH may be as high as 33%. may precipitate overt heart failure. hypertension is also thought to accelerate the process of aortic sclerosis and cause mitral regurgitation. Some degree of hemodynamically insignificant aortic insufficiency is often found in patients with uncontrolled hypertension. with return to baseline when the BP is better controlled.Stage C or D.Stage A or B. In addition to causing aortic regurgitation. per the ACC/AHA classification Hypertension as a cause of CHF is frequently underrecognized. leading to significant aortic insufficiency. Systolic dysfunction Later in the course of disease. these patients are predisposed to atrial fibrillation. leading to increases in salt and water retention and increased peripheral vasoconstriction. aging. It is often. the dysfunctioning left ventricle is unable to generate the high BP. chronic and severe hypertension can cause aortic root dilatation. thus obscuring the heart failure's etiology. accompanied by LVH. LV systolic function decreases further. but not invariably. with loss of atrial contribution in the presence of diastolic dysfunction. Valvular disease Although valvular disease does not cause hypertensive heart disease. systolic dysfunction. Diastolic dysfunction Diastolic dysfunction is common in persons with hypertension. In addition to elevated afterload. and the LV cavity begins to dilate to maintain cardiac output. This leads to further increases in activation of the neurohormonal and renin-angiotensin systems. the already compromised LV is overwhelmed. and the patient progresses to the stage of symptomatic systolic dysfunction. Chronically elevated afterload and the resulting LVH can adversely affect the active early relaxation phase and the late compliance phase of ventricular diastole. Eventually. partly because at the time heart failure develops.In addition to LA structural changes. An acute rise in BP may accentuate the degree of aortic insufficiency. other factors that may contribute to the development of diastolic dysfunction include coexistent coronary artery disease. . Patients with hypertension fall into 1 of the following categories: Asymptomatic but at risk of developing of heart failure . per the American College of Cardiology (ACC)/American Heart Association (AHA) classification. the LVH fails to compensate by increasing cardiac output in the face of elevated BP. depending on whether or not they have developed structural heart disease as a consequence of hypertension Suffering from symptomatic heart failure . and structural abnormalities such as fibrosis and LVH. Heart failure Heart failure is a common complication of chronically elevated BP. Atrial fibrillation. Asymptomatic systolic dysfunction usually follows. As the disease enters the end stage.
 In fact. compromising coronary blood flow during diastole. is exacerbated in arteries subjected to chronically elevated BP. A decreased nitric oxide level promotes the development and acceleration of arteriosclerosis and plaque formation. ischemia. The development and progression of arteriosclerosis. Hypertension is an established risk factor for the development of coronary artery disease. right ventricular (RV) thickening and diastolic dysfunction also develop as results of septal thickening and LV dysfunction. owing to changes in afterload conditions or to the presence of other insults to the myocardium (eg. Generally. Although the exact etiology is not known. or chronic persistent) is observed frequently in patients with hypertension. myocardial fibrosis. infarction). Shear stress associated with hypertension and the resulting endothelial dysfunction cause impairment in the synthesis and release of the potent vasodilator nitric oxide. Morphologic features of the plaque are identical to those observed in patients without hypertension. nearly 50% of patients with atrial fibrillation had hypertension. premature ventricular contractions (PVCs). The development of ischemia in patients with hypertension is multifactorial. Atrial fibrillation (paroxysmal. in patients with hypertension. A sudden increase in BP can lead to acute pulmonary edema without necessarily changing the LV ejection fraction. and it may be unable to compensate for increased metabolic and oxygen demand. All of these may lead to an increased risk of ventricular tachyarrhythmias. In addition. chronic recurrent. Increased afterload secondary to hypertension leads to an increase in LV wall tension and transmural pressure. elevated BP is the most common cause of atrial fibrillation in the Western hemisphere. The risk of sudden cardiac death is increased. The reason for this is 2-fold. angina can occur in the absence of epicardial coronary artery disease. Various mechanisms thought to play a part in the pathogenesis of arrhythmias include altered cellular structure and metabolism. In one study. and ventricular tachycardia (VT). LA structural abnormalities.Decompensation Apoptosis. poor perfusion. almost doubling the risk. associated coronary artery disease. the hallmark of coronary artery disease. inhomogeneity of the myocardium. In addition to LV dysfunction. and LVH have been suggested as possible contributing factors. stimulated by myocyte hypertrophy and the imbalance between its stimulants and inhibitors. the microvasculature beyond the epicardial coronary arteries has been shown to be dysfunctional in patients with hypertension. Importantly. is considered to play an important part in the transition from compensated to decompensated stage. development of asymptomatic or symptomatic LV dilatation or dysfunction heralds rapid deterioration in clinical status and a markedly increased risk of death. The patient may become symptomatic during the asymptomatic stages of the LV systolic or diastolic dysfunction. The development of atrial fibrillation can cause decompensation of . Cardiac arrhythmias Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation. Myocardial ischemia Patients with angina have a high prevalence of hypertension. or programmed cell death. and fluctuation in afterload.
a frequent complication of hypertensive heart disease. dietary indiscretion. especially atrial fibrillation. severity. Heart failure Although symptomatic diastolic heart failure and systolic heart failure are indistinguishable. ankle edema and weight gain. in severe cases. and it also increases the risk of thromboembolic complications. individuals who abruptly develop severe symptoms of CHF and rapidly return to baseline with medical therapy are more likely to have isolated diastolic dysfunction. or they can develop symptoms of heart failure insidiously over time. The etiology of these arrhythmias is thought to be concomitant coronary artery disease and myocardial fibrosis." Left ventricular hypertrophy Patients with LVH alone are totally asymptomatic. jaw. fatigue (more common in systolic dysfunction). upper back. unless the LVH leads to the development of diastolic dysfunction and heart failure. abdominal pain secondary to a congested. In particular. altered mentation. and/or squeezing Radiating to the neck.systolic and. Heart failure symptoms include exertional and nonexertional dyspnea (New York Heart Association [NYHA] classes I-IV). Patients can develop cardiac arrhythmias. owing to loss of atrial kick. the patient may or may not be aware of the presence of hypertension. This decompensation can be caused by precipitating factors such as an acute rise in BP. paroxysmal nocturnal dyspnea. more importantly. Premature ventricular contractions. and. Typical symptoms of angina include substernal chest pain lasting less than 15 minutes (vs >20min in infarction). is indistinguishable from other causes of myocardial ischemia. the clinical history may be quite revealing. pressure. Patient History Symptoms of hypertensive heart disease depend on the duration. or myocardial ischemia. In addition. Pain is often described as follows: A heaviness. orthopnea. Patients can present with acute pulmonary edema due to sudden decompensation in LV systolic or diastolic dysfunction. ventricular arrhythmias. and sudden cardiac death are observed more often in patients with LVH than in those without LVH. or left arm Provoked by emotional or physical exertion Relieved with rest or sublingual nitroglycerin . Myocardial ischemia Angina. distended liver. diastolic dysfunction. most notably stroke. which is why hypertension has been named "the silent killer. and type of disease.
Ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography. commonly referred to as an angina equivalent. stable angina or acute coronary syndrome. it is irregularly irregular if the patient is in atrial fibrillation. patients may also present with atypical symptoms without chest pain. The cardiac rhythm is regular if the patient is in sinus rhythm. are more likely to present atypically. including the following: Palpitations Near or total syncope Precipitation of angina Sudden cardiac death Precipitation of heart failure. the physical examination may reveal clues to a potential etiology of hypertension. in particular. In addition to generalized findings attributable directly to high BP. including myocardial infarction without ST-segment elevation and acute myocardial infarction with ST elevation. 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 . Acute coronary symptoms can be precipitated by a ruptured atherosclerotic plaque. and abdominal mass in polycystic kidney disease. Findings from the physical examination may be entirely normal in the very early stages of the disease.However. Patients may present with chronic. or the patient may have classic signs upon examination. such as exertional dyspnea or excessive fatigue. renal artery bruit in renal artery stenosis. such as truncal obesity and striae in Cushing syndrome. they can also result from an acute and severe rise in BP that leads to a sudden increase in transmural pressure without a change in stability of the plaque. Female patients. Cardiac arrhythmias Irregular or abnormal heart rhythms can cause a variety of symptoms. especially with atrial fibrillation in diastolic dysfunction Physical Examination Physical signs of hypertensive heart disease depend on the predominant cardiac abnormality and the duration and severity of the hypertensive heart disease. Pulses The arterial pulses are normal in the early stages of hypertensive heart disease.
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. owing to LV dilatation. 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. Veins In patients with heart failure. S1 is normal in intensity and character. decreased breath sounds. Later in the course of disease. In addition. the apical impulse is displaced laterally. when significant systolic LV dysfunction supervenes. it can have a reverse or paradoxical split due either to increased afterload or to associated left bundle-branch block (LBBB). such as rales. but it is decreased in patients with LV dysfunction. S4 is frequently palpable and audible. Lungs Findings upon chest examination may be normal or may include signs of pulmonary congestion. In the right ventricle. A holosystolic murmur of mitral regurgitation may be present in patients with advanced heart failure and a dilated mitral annulus. The predominant waves depend on the severity of the heart failure and any other associated lesions. a lift is present late in the course of heart failure if significant pulmonary hypertension develops. and dullness to percussion due to pleural effusion. frequently disappearing once the BP is better controlled. Abdomen .The pulse volume is usually normal. S3 is not typically present initially. especially in the presence of acutely elevated BP. Mean BP and pulse pressure are also elevated generally. an early systolic to midsystolic murmur of aortic sclerosis is commonly audible. A presystolic S4 may be felt. the jugular veins may be distended. Heart The apical impulse is sustained and nondisplaced in patients without significant systolic LV dysfunction but with LVH. S2 at the right upper sternal border is loud because of an accentuated aortic component (A2). 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). noncompliant ventricle due to chronic pressure overload and LVH. implying the presence of a stiffened. The BP in the upper extremities may be higher than that in the lower extremities in patients with coarctation of the aorta.
Category mm Hg mm Hg Optimal < 120 Prehypertension 120-139 Stage I 140-159 Stage II >160 < 80 80-89 90-99 >100 . Evaluation. Extremities Ankle edema may be present in patients with advanced heart failure. such as arteriovenous nicking. the severity of which depends on the duration and severity of the patient's hypertension. Detection. Table 1. Table 1. 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. and Treatment of High Blood Pressure (Open Table in a new window) Systolic BP. or earlier signs of hypertension. and hepatomegaly and ascites due to CHF.The abdominal examination may reveal a renal artery bruit in patients with hypertension secondary to renal artery stenosis. Examination of the fundi may reveal evidence of hypertensive retinopathy. below. shows the division of BP and hypertension into 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. Diastolic BP. a pulsatile expansile mass of abdominal aortic aneurysm. Stages of Elevated BP and Hypertension According to The Seventh Report of the Joint National Committee (JNC7) on Prevention. Staging of Hypertension Although hypertensive heart disease typically is not described in various stages. and cardiovascular mortality are increased in patients once LVH develops and are also increased in patients with heart failure. sudden cardiac death. ventricular arrhythmias. CNS changes may also be seen in patients who present with hypertensive emergency.
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. and triglycerides Optional tests . ischemic ECG changes may be found in individuals presenting with hypertensive crisis in whom no significant coronary atherosclerosis is detectable by coronary angiography. Evaluating the endocrine system Hypokalemia is found in patients with primary hyperaldosteronism and in patients with secondary hyperaldosteronism.Laboratory Studies Laboratory studies are helpful in establishing the etiology of hypertension.Includes high density lipoprotein (HDL) cholesterol. Plasma renin activity is generally depressed and serum aldosterone level is elevated in patients with primary hyperaldosteronism. Hypokalemia is most useful in leading to further diagnostic studies if the patient has not received diuretics.) . 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. Recommendations from the Seventh Report of the Joint National Committee (JNC7) on Prevention. GFR. Electrocardiography A 12-lead ECG may show a variety of abnormalities. and Treatment of High Blood Pressure include carrying out the following baseline laboratory workup before initiating treatment for hypertension : Electrocardiogram Urinalysis Blood glucose and hematocrit levels Serum potassium. low-density lipoprotein (LDL) cholesterol. Twenty-four – hour urinary catecholamine and metanephrine levels are elevated in patients with pheochromocytoma. Cushing disease. creatinine (or the corresponding estimated glomerular filtration rate [GFR]). Evidence of LA enlargement includes broad P waves in the limb leads and a prominent and wide. and monitoring the adverse effects of therapy. and calcium measurements Lipid profile after a 9. delayed negative deflection in V1. The tests to be ordered depend on clinical judgment regarding the etiology of hypertension. Other studies include the above-mentioned urinalysis. For example. and Bartter syndrome. Evaluation. and urinary albumin excretion or albumin/creatinine ratio measurements. (See the images below. Thyrotropin levels may be elevated in patients with hypothyroidism and depressed in patients with hyperthyroidism. Detection.to 12-hour fast . quantitating the severity of target organ damage.
among patients with left anterior fascicular block on ECG. Electrocardiogram from a 46-year-old man with long-standing hypertension showing left atrial abnormality and left ventricular hypertrophy with strain. 50% had hypertension. In one series. As many as 70-80% of patients with LBBB have hypertension. LVH criteria .Electrocardiogram from a 47-year-old man with a long-standing history of uncontrolled hypertension showing left atrial enlargement and left ventricular hypertrophy.
the Romhilt-Estes criteria. Romhilt-Estes Criteria (A Point Score System*) (Open Table in a new window) Voltage Criteria R wave or S wave in any limb lead >0. The sensitivity of these criteria is 50%. with a specificity of close to 95%. for example. The frequency of LVH on ECG at the time of initial diagnosis varies from 10% to 100%.6mV.2mV or S wave in lead V1 or V2 or R wave in V5 or V6 >0. The sensitivity of these criteria is 25%. differing in sensitivity and specificity. Note that the specificities and sensitivities of the different approaches are far less than those of echocardiography. .05 seconds * Points 3 3 1 3 2 1 1 Probable LVH is 4 points. definite LVH is 5 points. The Cornell criteria (most sensitive) are (1) R wave in aVL plus an S wave in V3 of greater than 2. with a specificity of close to 95%. Table 2. The Gubner-Ungerleider criteria are an R wave in I plus an S wave in III of greater than 2.09 seconds Intrinsicoid deflection in V5 or V6 >0.8 mV in men and greater than 2mV in women.04 seconds wide) Left-axis deviation greater than -30° QRS duration greater than 0. Another set of LVH criteria. A Cornell voltage duration of greater than 2440mV/ms-1 particularly identifies the highest-risk patients. The sensitivity of ECG for diagnosing LVH is limited. 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%. the frequency was 13%.1mV deep and 0. are summarized in Table 2.3mV LV strain (ST and T waves in direction opposite to QRS direction) without digitalis LV strain (ST and T waves in direction opposite to QRS direction) with digitalis LA enlargement (terminal negativity of P waves in V1 >0. The Sokolow-Lyon criteria are an S wave in V1 plus an R wave in V5 or V6 of greater than 3. approximately 30-57% in patients with severe LVH.5mV. in one trial. below.5mV or an R wave in V5 or V6 of greater than 2. have been used to diagnose LVH.Various criteria.