Hypertrophy, cardiac left ventricular

Lewis BS, Gotsman MS (1975) Cardiac hypertrophy and left ventricular end-diastolic stress. Israel J Med Sci 11 299-303... 

Ter Keurs HEDJ, Schipperheyn JJ, eds Cardiac left ventricular hypertrophy. 1983. ISBN 0-89838-612-8. Sperelakis N, ed Physiology and pathophysiology of the heart. ISBN 0-89838-615-2. 

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. 

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. 

ACE-inhibitors are known to cause regression of left ventricular and vascular hypertrophy. This phenomenon is important in the long-term treatment of hypertension, where cardiac hypertrophy is known to be an important, virtually independent risk factor. Data that are beginning to emerge, which indicate that ACE-inhibitors may be beneficial as secondary prevention in postinfarct patients, especially if signs of heart failure occur. This favourable influence of the ACE-inhibitors may be the result of haemodynamic effects, a favourable effect on neuroendocrine mechanisms, and also a beneficial influence on the process of remodeling of the heart, secondary to a myocardial infarction. 

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 ... 

The heart may be enlarged with left ventricular hypertrophy, particularly in cases which have exhibited hypertension during life. Metastatic calcification of the valves and of the myocardium may be present, explaining no doubt the cardiac murmurs which may have been detected clinically in such cases. Occasionally, medullary proliferation of large arteries and, in the smaller arteries, fragmentation of the intimal elastic lamina has been reported, in one case with impregnation with calcium salts. Local calcification of the media of the middle cerebral artery has been described. 

Galinier, M., Senard, J.M., Valet, P., Arias, A., Daviaud, D., Clock, Y., Bounhoure, J.P., and Montastruc, J.L. 1994. Cardiac p-adrenoceptors and adenylyl cyclase activity in human left ventricular hypertrophy due to pressure overload. Fundam. Clin. Pharmacol. 8 90-99. 

Ichihara, S., Senbonmatsu, T., Price, E., Jr., et al. 2001. Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic angiotensin II-induced hypertension. Circulation 104 346-351. 

Adverse effects Thiazide diuretics induce hypokalemia and hyperuricemia in 70% of patients, and hyperglycemia in 10% of patients. Serum potassium levels should be monitored closely in patients who are predisposed to cardiac arrhythmias (particularly individuals with left ventricular hypertrophy, ischemic heart disease, or chronic congestive heart failure) and who are concurrently being treated with both thiazide diuretics and digitalis glycosides (see p. 160). Diuretics should be avoided in the treatment of hypertensive diabetics or patients with hyperlipidemia. 

A 57-year-old man with bipolar disorder taking olanzapine, lithium, and other drugs had underlying mitral valve prolapse, left ventricular hypertrophy, and His bundle anomalies he died suddenly, probably because of a cardiac dysrhythmia. 

Coronary heart disease is associated with ischemic stroke in postmortem (Stemmermann et al. 1984), twin (Brass et al. 1996), case-control (Feigin et al. 1998) and cohort studies (Harmsen et al. 1990 Shaper et al. 1991 Wolf et al. 1991b Touze et al. 2006) as are electrocardiographic abnormalities, cardiac failure, left ventricular hypertrophy, claudication and asymptomatic peripheral vascular disease (Leys et al. 2006). 

Thorough cardiac examination should look for possible cardiac source of embolism, including atrial fibrillation, mitral stenosis and prosthetic heart valves. Left ventricular hypertrophy suggests hypertension or aortic stenosis, and a displaced apex from a dilated left ventricle indicates underlying cardiac or valvular pathology. 

Severe recurrent, but usually reversible hjrpertrophic cardiomyopathy has been infrequently reported, both in adults and children (SEDA-19, 352) (SEDA-20, 346). Based on experimental data and one additional case report, the interaction of tacrolimus with calcium channel blockers in the cardiac muscle has been suggested as a possible mechanism (SEDA-21, 390). However, the role of tacrolimus in the development of cardiomyopathy is still hjrpothetical. Echocardiographic abnormalities were relatively common before and after liver transplantation in 12 adult patients, and there was no clear evidence that oral tacrolimus specifically alters cardiac function (13). Other investigators did not show differences in heart weight, ventricular thickness, or valve circumferences between 67 Uver transplant recipients treated with tacrolimus and 72 non-transplanted patients who died from end-stage liver disease (14). In addition, more than 80% of patients in both groups had left ventricular hypertrophy. 

Fig. 3. a1A-AR overexpression induces enhanced contractility but not cardiac hypertrophy. (A) Representative left ventricular pressure (LVP) and dP/dT tracings from transgenic animals (TG) and nontransgenic littermates (NTL). A slower recording speed is shown at the beginning. (B) In vivo effects of ISO administration before and after complete P-AR blockade with propanolol (left panel) in NTL (open square) and TG (closed square) mice. Effects of selective a1A-AR blocker KMD3213 on +dP/dT and -dP/ dT are shown in the right panel. (From ref. 29 2001 Lippincott Williams Wilkins.)... 

Anemia has both direct and indirect effects on left ventricular function and growth. Cardiac output increases because of a combination of increased cardiac preload and a reduction in afterload. Such changes lead to ventricular remodeling, with initial left ventricular dilation followed by subsequent hypertrophy. In ESRD other factors also contribute to LVH, including hypertension, volume expansion, and the metabolic consequences of uremia, to which maybe added the effects of diabetes. By the time patients with diabetes reach ESRD, they are more likely to have concentric LVH, more likely to have had ischemic heart disease, and more likely to have experienced cardiac failure than nondiabetic subjects. ... 

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