Ventricular hypertrophy

ACE inhibitors lower the elevated blood pressure in humans with a concomitant decrease in total peripheral resistance. Cardiac output is increased or unchanged heart rate is unchanged urinary sodium excretion is unchanged and potassium excretion is decreased. ACE inhibitors promote reduction of left ventricular hypertrophy. 

Methyldopa is effective in mild, moderate, and severe hypertension but a thiazide-type diuretic is needed to overcome the fluid retaining side effect. Methyldopa has been shown to prevent and induce regression of ventricular hypertrophy in hypertensive patients. The principal side effects are sedation, drowsiness, nasal congestion, fluid retention, and in rare occasions, hemolytic anemia. 

Patients with diabetes and hypertension should initially be treated with either P-blockers, ACE inhibitors, ARBs, diuretics, or calcium channel blockers. There is a general consensus that therapy focused on RAAS inhibition by ACE inhibitors or ARBs may be optimal if the patient has additional cardiovascular risk factors such as left ventricular hypertrophy or chronic kidney disease.2,3,59,67... 

Ventricular hypertrophy (e.g., hypertrophic cardiomyopathy, other examples above)... 

Ventricular hypertrophy Maintains cardiac output Diastolic dysfunction... 

To reduce mortality, administration of an aldosterone antagonist, either eplerenone or spironolactone, should be considered within the first 2 weeks following MI in all patients who are already receiving an ACE inhibitor (or ARB) and have an EF of equal to or less than 40% and either heart failure symptoms or diagnosis of diabetes mellitus.3 Aldosterone plays an important role in heart failure and in MI because it promotes vascular and myocardial fibrosis, endothelial dysfunction, hypertension, left ventricular hypertrophy, sodium retention, potassium and magnesium loss, and arrhythmias. Aldosterone antagonists have been shown in experimental and human studies to attenuate these adverse effects.70 Spironolactone decreases all-cause mortality in patients with stable, severe heart failure.71... 

CAD, coronary artery disease LVEF, left ventricular ejection fraction LVH, left ventricular hypertrophy. (Algorithm adapted with permission from Tisdale JE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, Dunsworth TS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 217-267.)50... 

Cardiovascular Worsening hypertension, edema, dyslipi-demia, left ventricular hypertrophy, electrocardiographic changes and chronic heart failure. 

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

Cardiovascular Left ventricular hypertrophy, ECG changes, congestive heart failure Neurologic Impaired mental cognition Genitourinary Sexual dysfunction... 

Cardiovascular diseases hypertension, coronary heart disease, cardiomyopathy, left ventricular hypertrophy, and arrhythmia. 

LVH Left ventricular hypertrophy tion no venereal disease nonvalvular disease... 

PRN When necessary, as needed (pro re nata) RVH Right ventricular hypertrophy... 

Myerson SG, Montgomery HE, Whit-TINGHAM M, JUBB M, WORLD MJ, Humphries SE, Pennelll DJ. Left ventricular hypertrophy with exercise and ACE gene insertion/deletion polymorphism - a randomized controlled trial with losartan. Circulation 2001 103 226-230. 

The answer is a. (Hardman, pp 762-764.) Experimentally, nitrates dilate coronary vessels. This occurs in normal subjects, resulting in an overall increase in coronary blood flow. In arteriosclerotic coronaries, the ability to dilate is lost, and the ischemic area may actually have less blood flow under the influence of nitrates. Improvement in the ischemic conditions is the result of decreased myocardial oxygen demand because of a reduction of preload and afterload. Nitrates dilate both arteries and veins and thereby reduce the work of the heart. Should systemic blood pressure fall, a reflex tachycardia will occur. In pure coronary spasm, such as Prinzmetal s angina, the effect of increased coronary blood flow is relevant, while in severe left ventricular hypertrophy with minimal obstruction, the effect on preload and afterload becomes important. 

Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states). 

Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and infarction, mitral or tricuspid valve stenosis, and pericardial disease (e.g., pericarditis, pericardial tamponade). 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

Ventricular hypertrophy can be demonstrated on chest x-ray or ECG. Chest x-ray may also show pleural effusions or pulmonary edema. 

Previous Ml, left ventricular hypertrophy, left ventricular systolic dysfunction... 

The ACE gene encodes two isozymes (somatic ACE isozyme and germinal ACE isozyme). ACE is a membrane-bound enzyme on the surface of vascular endothelial cells that also circulates in plasma and shows great individual variability determined by an I/D polymorphism in intron 16 of the ACE gene (ACE-I/D polymorphism). More than 160 ACE polymorphisms have been reported, 34 of which are located in coding regions, and 18 are missense mutations (606). ACE-related polymorphic variants have been associated with hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic renal failure in IgA nephropathy, Henoch-Schonlein purpura nephritis, mechanical efficiency of skeletal muscle, intracranial aneurysms, susceptibility to myocardial infarction, diabetic nephropathy, AD, and longevity (12,606,607). 

Somatomedins are insulin-like polypeptide hormones that should be used with caution in diabetic patients since adjustment of antidiabetic therapy may be required. Before initiating therapy, a baseline ECG is recommended and, if abnormalities are identified, regular ECG monitoring during treatment is required. Somatomedins may cause tachycardia, cardiomegaly, ventricular hypertrophy and changes in blood glucose levels as side-effects. 

Hypertensive patients with ieft ventricuiar hypertrophy (iosartan) Used to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy, but there is evidence that this benefit does not apply to black patients. 

Left ventricular hypertrophy Angina or prior myocardial infarction Prior coronary revascularization Heart failure... 

ARBs Type 2 diabetic nephropathy Type 2 diabetic microalbuminuria Proteinuria Left ventricular hypertrophy ACE-I cough or intolerance Pregnancy Hyperkalaemia Bilateral renal artery stenosis ... 

Administration of one of the jS-blockers and an ACE-I is mandatory for all patients with a recent MI, regardless of the ejection fraction (EE). If the LVEE is reduced in patients without a history of MI, yS-blockers and/or ACE-I should be administrated as long as the patients do not have heart failure symptoms. If an ACE-I is contraindicated, it has to be substituted by an ARB, if the patient is post-MI with low EE, but no manifest HF. This may also be true without a history of MI. ACE-I and ARB are beneficiary for those with hypertension and left ventricular hypertrophy (LVH), without HF symptoms. 

The management of heart failure in the presence of normal systolic function is not reviewed. This form of heart failure commonly occurs in the elderly with chronic hypertension and left ventricular hypertrophy. The failure of the left ventricle to relax during diastole (diastolic dysfunction) results in elevated end diastolic... 

Julie Singer is a 55-year-old white woman who was admitted to the emergency department in acute distress. A previous physical examination showed hypertension and diabetes mellitus type 2. The patient s present medications include enalapril 40 mg, nifedipine 60 mg, and 100 U insulin. A physical examination revealed prominent ankle edema, a palpable spleen, and hepatomegaly. Chest radiography revealed diffuse cardiac enlargement and left ventricular hypertrophy. Based upon the history and clinical hndings, what is your diagnosis and what treatment do you recommend ... 

Diets containing corn oil, coconut oil and cholesterol alter ventricular hypertrophy, dilatation and function in hearts of rats fed copper-deficient diets. J Nutr 1993 123(6) 1150-1160. 

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