BAB II

BAB II

PEMBAHASAN

II.1.DefinisiPenyakit jantung hipertensi merupakan suatu penyakit yang berkaitan dengan dampak sekunder pada jantung karena hipertensi sistemik yang lama dan berkepanjangan. Sampai saat ini prevalensi hipertensi di Indonesia berkisar antara 5-10%. Sejumlah 85-90% hipertensi tidak diketahui penyebabnya atau disebut sebagai hipertensi primer (hipertensi esensial atau idiopatik). Sejumlah 85-90 % hipertensi tidak diketahui penyebabnya atau disebut sebagai hipertensi primer (hipertensi esensial atau Idiopatik). Hanya sebagian kecil hipertensi yang dapat ditetapkan penyebabnya (hipertensi sekunder).Tidak ada data akurat mengenai prevalensi hipertensi sekunder dan sangat tergantung di mana angka itu diteliti. Diperkirakan terdapat sekitar 6% pasien hipertensi sekunder sedangkan di pusat rujukan dapat mencapai sekitar 35%. Hampir semua hipertensi sekunder didasarkan pada 2 mekanisme yaitu gangguan sekresi hormon dan gangguan fungsi ginjal. Pasien hipertensi sering meninggal dini karena komplikasi jantung (yang disebut sebagai penyakit jantung hipertensi). Juga dapat menyebabkan strok, gagal ginjal, atau gangguan retina mata.(papdi)(transletkan!!!) (kurang, tambah sumber lagi)Hypertensive heart disease is a late complication of hypertension (high blood pressure) in which the heart is affected. (sumber: http://www.umm.edu/ency/article/000163.htm)II.2.Etiologi

High blood pressure increases the heart's workload, and over time, this can cause the heart muscle to thicken. As the heart pumps against elevated pressure in the blood vessels, the left ventricle becomes enlarged and the amount of blood pumped by the heart each minute (cardiac output) goes down. Without treatment, symptoms of congestive heart failure may develop.

High blood pressure is the most common risk factor for heart disease and stroke. It can cause ischemic heart disease (decreased blood to the heart muscle that results in anginal chest pain and heart attacks) from the increased supply of oxygen needed by the thicker heart muscle.

High blood pressure also contributes to thickening of the blood vessel walls, which in turn may aggravate atherosclerosis (increased cholesterol deposits in the blood vessels). This also increases the risk of heart attacks and stroke. Hypertensive heart disease is the leading cause of illness and death from hypertension. It affects approximately 7 out of 1,000 people. (sumber: http://www.umm.edu/ency/article/000163.htm)II.3. KlasifikasiII.4.PatofisiologiThe pathophysiology of hypertensive heart disease is a complex interplay of various hemodynamic, structural, neuroendocrine, cellular, and molecular factors. On 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 hypertrophyOf patients with hypertension, 15-20% develop LVH. The risk of LVH is increased 2-fold by associated obesity. The prevalence of LVH based on ECG findings, which are not a sensitive marker at the time of diagnosis of hypertension, is variable. 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 (Some of the genes are given expression primarily in fetal cardiomyocytes.), and, thus, 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. Thus, 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. Compare this with eccentric LVH, in which LV thickness is increased not uniformly but at certain sites, such as the septum. Concentric LVH is a marker of poor prognosis in the presence of hypertension. 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 abnormalitiesFrequently 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 diseaseAlthough 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 failureHeart 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 usually, 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. 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 ischemiaPatients 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 arrhythmiasCardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation, premature ventricular contractions, and ventricular tachycardia.The risk of sudden cardiac death is increased. 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. 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.

(sumber: http://www.emedicine.com/MED/topic3432.htm)II.5.Diagnosis

HistoryThe initial assessment of the hypertensive patient should include a complete history and physical examination to confirm a diagnosis of hypertension, screen for other cardiovascular disease risk factors, screen for secondary causes of hypertension, identify cardiovascular consequences of hypertension and other comorbidities, assess blood pressurerelated lifestyles, and determine the potential for intervention. Most patients with hypertension have no specific symptoms referable to their blood pressure elevation. Although popularly considered a symptom of elevated arterial pressure, headache generally occurs only in patients with severe hypertension. Characteristically, a "hypertensive headache" occurs in the morning and is localized to the occipital region. Other nonspecific symptoms that may be related to elevated blood pressure include dizziness, palpitations, easy fatigability, and impotence. When symptoms are present, they are generally related to hypertensive cardiovascular disease or to manifestations of secondary hypertension. Table 241-5 lists salient features that should be addressed in obtaining a history from a hypertensive patient.

Table 241-5 Patient's Relevant History

Duration of hypertension

Previous therapies: responses and side effects

Family history of hypertension and cardiovascular disease

Dietary and psychosocial history

Other risk factors: weight change, dyslipidemia, smoking, diabetes, physical inactivity

Evidence of secondary hypertension: history of renal disease; change in appearance; muscle weakness; spells of sweating, palpitations, tremor; erratic sleep, snoring, daytime somnolence; symptoms of hypo- or hyperthyroidism; use of agents that may increase blood pressure

Evidence of target organ damage: history of TIA, stroke, transient blindness; angina, myocardial infarction, congestive heart failure; sexual function

Other comorbidities

Note: TIA, transient ischemic attack.

Measurement of Blood PressureReliable measurements of blood pressure depend on attention to the details of the technique and conditions of the measurement. Owing to recent regulations preventing the use of mercury because of concerns about its potential toxicity, most office measurements are made with aneroid instruments. The accuracy of automated blood pressure instruments should be confirmed. Before taking the blood pressure measurement, the individual should be seated quietly for 5 min in a private, quiet setting with a comfortable room temperature. The center of the cuff should be at heart level, and the width of the bladder cuff should equal at least 40% of the arm circumference; the length of the cuff bladder should encircle at least 80% of the arm circumference. It is important to pay attention to cuff placement, stethoscope placement, and the rate of deflation of the cuff (2 mmHg/s). Systolic blood pressure is the first of at least two regular "tapping" Korotkoff sounds, and diastolic blood pressure is the point at which the last regular Korotkoff sound is heard. In current practice, a diagnosis of hypertension is generally based on seated, office measurements.Currently available ambulatory monitors are fully automated, use the oscillometric technique, and typically are programmed to take readings every 1530 min. Ambulatory blood pressure monitoring is not, however, routinely used in clinical practice and is generally reserved for patients in whom white coat hypertension is suspected. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) has also recommended ambulatory monitoring for treatment resistance, symptomatic hypotension, autonomic failure, and episodic hypertension.Physical ExaminationBody habitus, including weight and height, should be noted. At the initial examination, blood pressure should be measured in both arms, and preferably in the supine, sitting, and standing positions to evaluate for postural hypotension. Even if the femoral pulse is normal to palpation, arterial pressure should be measured at least once in the lower extremity in patients in whom hypertension is discovered before age 30. Heart rate should also be recorded. Hypertensive individuals have an increased prevalence of atrial fibrillation. The neck should be palpated for an enlarged thyroid gland, and patients should be assessed for signs of hypo- and hyperthyroidism. Examination of blood vessels may provide clues about underlying vascular disease and should include funduscopic examination, auscultation for bruits over the carotid and femoral arteries, and palpation of femoral and pedal pulses. The retina is the only tissue in which arteries and arterioles can be examined directly. With increasing severity of hypertension and atherosclerotic disease, progressive funduscopic changes include increased arteriolar light reflex, arteriovenous crossing defects, hemorrhages and exudates, and, in patients with malignant hypertension, papilledema. Examination of the heart may reveal a loud second heart sound due to closure of the aortic valve and an S4 gallop, attributed to atrial contraction against a noncompliant left ventricle. Left ventricular hypertrophy may be detected by an enlarged, sustained, and laterally displaced apical impulse. An abdominal bruit, particularly a bruit that lateralizes and extends throughout systole into diastole, raises the possibility of renovascular hypertension. Kidneys of patients with polycystic kidney disease may be palpable in the abdomen. The physical examination should also include evaluation for signs of CHF and a neurologic examination.

Laboratory TestingTable 241-6 lists recommended laboratory tests in the initial evaluation of hypertensive patients. Repeat measurements of renal function, serum electrolytes, fasting glucose, and lipids may be obtained after introducing a new antihypertensive agent and then annually, or more frequently if clinically indicated. More extensive laboratory testing is appropriate for patients with apparent drug-resistant hypertension or when the clinical evaluation suggests a secondary form of hypertension.

Table 241-6 Basic Laboratory Tests for Initial Evaluation

System

Test

Renal

Microscopic urinalysis, albumin excretion, serum BUN and/or creatinine

Endocrine

Serum sodium, potassium, calcium, ?TSH

Metabolic

Fasting blood glucose, total cholesterol, HDL and LDL (often computed) cholesterol, triglycerides

Other

Hematocrit, electrocardiogram

Note: BUN, blood urea nitrogen; TSH, thyroid-stimulating hormone; HDL, LDL, high-/low-density lipoprotein

(Sumber: Harrison Iqbal)II.6.PenatalaksanaanLifestyle InterventionsImplementation of lifestyles that favorably affect blood pressure has implications for both the prevention and treatment of hypertension. Health-promoting lifestyle modifications are recommended for individuals with pre-hypertension and as an adjunct to drug therapy in hypertensive individuals. These interventions should address overall cardiovascular disease risk. Although the impact of lifestyle interventions on blood pressure is more pronounced in persons with hypertension, in short-term trials, weight loss and reduction of dietary NaCl have also been shown to prevent the development of hypertension. In hypertensive individuals, even if these interventions do not produce a sufficient reduction of blood pressure to avoid drug therapy, the number of medications or dosages required for blood pressure control may be reduced. Dietary modifications that effectively lower blood pressure are weight loss, reduced NaCl intake, increased potassium intake, moderation of alcohol consumption, and an overall healthy dietary pattern (Table 241-7).

Table 241-7 Lifestyle Modifications to Manage Hypertension

Weight reduction

Attain and maintain BMI < 25 kg/m2

Dietary salt reduction

< 6 g NaCl/d

Adapt DASH-type dietary plan

Diet rich in fruits, vegetables, and low-fat dairy products with reduced content of saturated and total fat

Moderation of alcohol consumption

For those who drink alcohol, consume 2 drinks/day in men and 1 drink/day in women

Physical activity

Regular aerobic activity, e.g., brisk walking for 30 min/d

Note: BMI, body mass index; DASH, Dietary Approaches to Stop Hypertension (trial).

Prevention and treatment of obesity are important for reducing blood pressure and cardiovascular disease risk. In short-term trials, even modest weight loss can lead to a reduction of blood pressure and an increase of insulin sensitivity. Average blood pressure reductions of 6.3/3.1 mmHg have been observed with a reduction in mean body weight of 9.2 kg. Regular physical activity facilitates weight loss, decreases blood pressure, and reduces the overall risk of cardiovascular disease. Blood pressure may be lowered by 30 min of moderately intense physical activity, such as brisk walking, 67 days a week, or by more intense, less frequent workouts.

There is individual variability in the sensitivity of blood pressure to NaCl, and this variability may have a genetic basis. Based on results of meta-analyses, lowering of blood pressure by limiting daily NaCl intake to 4.47.4 g (75125 meq) results in blood pressure reductions of 3.74.9/0.92.9 mmHg in hypertensive and lesser reductions in normotensive individuals. Diets deficient in potassium, calcium, and magnesium are associated with higher blood pressures and a higher prevalence of hypertension. The urine sodium-to-potassium ratio is a stronger correlate of blood pressure than either sodium or potassium alone. Potassium and calcium supplementation have inconsistent, modest antihypertensive effects, and, independent of blood pressure, potassium supplementation may be associated with reduced stroke mortality. Alcohol use in persons consuming three or more drinks per day (a standard drink contains ~14 g ethanol) is associated with higher blood pressures, and a reduction of alcohol consumption is associated with a reduction of blood pressure. Mechanisms by which dietary potassium, calcium, or alcohol may affect blood pressure have not been established.

The DASH (Dietary Approaches to Stop Hypertension) trial convincingly demonstrated that over an 8-week period a diet high in fruits, vegetables, and low-fat dairy products lowers blood pressure in individuals with high-normal blood pressures or mild hypertension. Reduction of daily NaCl intake to 50%. There is considerable variation in individual responses to different classes of antihypertensive agents, and the magnitude of response to any single agent may be limited by activation of counterregulatory mechanisms that oppose the hypotensive effect of the agent. Selection of antihypertensive agents, and combinations of agents, should be individualized, taking into account age, severity of hypertension, other cardiovascular disease risk factors, comorbid conditions, and practical considerations related to cost, side effects, and frequency of dosing.

Diuretics

Low-dose thiazide diuretics are often used as first-line agents, alone or in combination with other antihypertensive drugs. Thiazides inhibit the Na+/Cl pump in the distal convoluted tubule and, hence, increase sodium excretion. Long term, they may also act as vasodilators. Thiazides are safe, efficacious, and inexpensive and reduce clinical events. They provide additive blood pressurelowering effects when combined with beta blockers, ACE inhibitors, or angiotensin receptor blockers. In contrast, addition of a diuretic to a calcium channel blocker is less effective. Usual doses of hydrochlorothiazide range from 6.2550 mg/d. Owing to an increased incidence of metabolic side effects (hypokalemia, insulin resistance, increased cholesterol), higher doses are generally not recommended. Two potassium-sparing diuretics, amiloride and triamterene, act by inhibiting epithelial sodium channels in the distal nephron. These agents are weak antihypertensive agents but may be used in combination with a thiazide to protect against hypokalemia. The main pharmacologic target for loop diuretics is the Na+-K+-2Cl cotransporter in the thick ascending limb of the loop of Henle. Loop diuretics are generally reserved for hypertensive patients with reduced glomerular filtration rates [reflected serum creatinine >220 mol/L (>2.5 mg/dL], CHF, or sodium retention and edema for some other reason such as treatment with a potent vasodilator, e.g., minoxidil.

Blokers of The Renin-Angiotensin System

ACE inhibitors decrease the production of angiotensin II, increase bradykinin levels, and reduce sympathetic nervous system activity. Angiotensin II receptor blockers provide selective blockade of AT1 receptors, and the effect of angiotensin II on unblocked AT2 receptors may augment the hypotensive effect. Both classes of agents are effective antihypertensive agents that may be used as monotherapy or in combination with diuretics, calcium antagonists, and alpha-blocking agents. Side effects of ACE inhibitors and angiotensin receptor blockers include functional renal insufficiency due to efferent renal arteriolar dilatation in a kidney with a stenotic lesion of the renal artery. Additional predisposing conditions to renal insufficiency induced by these agents include dehydration, CHF, and use of nonsteroidal anti-inflammatory drugs. Dry cough occurs in ~15% of patients, and angioedema occurs in