Left ventricular hypertrophy: impact of calcium channel blocker therapy

Article Abstract:

Left ventricular hypertrophy (LVH) is an increase in the muscle mass of the left ventricle of the heart (the chamber from which blood is pumped to all portions of the body except the lungs). This condition, which is a frequent adaptation seen in patients with sustained hypertension (high blood pressure), was once thought to be a beneficial compensation by the heart to the stress of increased blood pressure that served to partially normalize cardiovascular function. It has since been documented that patients with LVH are at increased risk of sudden death and heart attack over those without LVH, regardless of blood pressure. Frequent adverse effects of LVH include ventricular ectopy (irregular contractions of the left ventricle), impaired ability of the ventricle to contract, myocardial ischemia (a reduction in blood supply to the heart), and decreased ventricular filling (a decrease in the volume of blood going into the left ventricle prior to contraction). A variety of drugs are used to treat hypertension, including diuretics, beta adrenergic receptor antagonists, angiotensin converting-enzyme (ACE) inhibitors, and calcium channel blockers. A desirable consequence of antihypertensive therapy is that it should not only reduce blood pressure, but it should also reduce the occurrence of the adverse conditions associated with hypertension. In this regard, it has been shown that when patients are given either calcium channel blockers or diuretics (in doses that cause equivalent reductions in blood pressure), only the calcium channel blockers reduce both LVH and irregular ventricular contraction; diuretic treatment was ineffective in altering either of these factors. (Consumer Summary produced by Reliance Medical Information, Inc.)

Heart enlargement, Heart hypertrophy

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Relation of obesity, high sodium intake, and eccentric left ventricular hypertrophy to left ventricular exercise dysfunction in essential hypertension

Article Abstract:

Hypertension (high blood pressure) increases the risk of congestive heart failure, the inability of the heart to pump blood, which results in congestion of the lungs. However, there are no methods to identify impaired function of the heart in hypertensive patients at a stage when the damage could be reversed. Studies have shown that a certain proportion of hypertensive patients have impaired heart functions during exercise. The factors contributing to impaired function of the left ventricle during exercise were assessed among 127 hypertensive patients. The patients were examined by angiography (X-ray of the blood vessels) both at rest and during exercise, and by echocardiography (the use of ultrasound waves to visualize heart structures) at rest. Twenty-four patients had less-than-normal left ventricular ejection fractions, the relative percentage of blood emptied from the left ventricle at the end of contraction, used as a measure of contractility. Although age and blood pressures at rest and during exercise were similar among all patients, patients with subnormal left ventricular ejection fraction tended to be obese. Impaired function of the left ventricle was associated with increases in size of the left ventricle; tension on the wall of the heart at the end of contraction; dietary sodium intake; and body weight. The results show that impaired function of the heart during exercise in hypertensive patients is associated with enlargement of the left ventricle, obesity, and high sodium intake. (Consumer Summary produced by Reliance Medical Information, Inc.)

Analysis, Risk factors, Physiological aspects, Heart failure, Exercise tests, Heart function tests

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Nephron heterogeneity: clue to the pathogenesis of essential hypertension and effectiveness of angiotensin-converting enzyme inhibitor treatment

Article Abstract:

The enzyme renin is produced by the kidneys. Renin converts the blood protein angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasopressor, in that it constricts blood vessels, and also increases the production and release of the mineralocorticoid hormone aldosterone from the adrenal glands. Aldosterone increases sodium retention. Agents which prevent the action of ACE and the formation of angiotensin II have been used to treat hypertension, or abnormally high blood pressure. Essential hypertension, high blood pressure due to unknown cause, is associated with two types of abnormally functioning nephrons, the structural and functional units of the kidney. One nephron type is ischemic, or lacking a sufficient blood supply, and releases large amounts of renin but low amounts of sodium. The other type of nephron excretes high amounts of sodium, but releases decreased levels of renin. The combined effects of these nephrons may result in the deceptively "normal" glomerular filtration rate, or rate at which blood is filtered through the kidney, and "normal" blood levels of renin. The large amount of renin released by the ischemic nephrons has different effects on the two types of nephrons that contribute to the development of hypertension. ACE inhibitors, which specifically prevent reactions occurring after renin action, are effective in lowering blood pressure even when renin levels are not elevated. (Consumer Summary produced by Reliance Medical Information, Inc.)

Abnormalities, Drug therapy, ACE inhibitors, Angiotensin converting enzyme inhibitors, Kidney tubules, Renal tubule, Essential hypertension

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