Myocardial hypertrophy

Methyldopa. Methyldopa reduces arterial blood pressure by decreasing adrenergic outflow and decreasing total peripheral resistance and heart rate having no change in cardiac output. Blood flow to the kidneys is not changed and that to the heart is increased. It causes regression of myocardial hypertrophy. 

History of clinically significant heart disease (e.g. myocardial hypertrophy, heart failure)... 

Myocardial hypertrophy Myocardial hypertrophy has been reported in association with the administration of tacrolimus and generally is manifested by echocardiographically demonstrated concentric increases in left ventricular posterior wall and interventricular septum thickness. Hypertrophy has been observed in infants, children, and adults. This condition appears reversible in most cases following dose reduction or discontinuance of therapy. 

These drugs have potential for the treatment of hypertension, myocardial hypertrophy, and other diseases. 

Patients should be informed of the need for regular laboratory monitoring Myocardial hypertrophy Pregnancy Category C... 

There is a risk of myocardial hypertrophy in children on prolonged treatment with ACTH (2), an effect that could reflect increased androgen secretion and thus be more likely to occur than with glucocorticoids. 

There is evidence that by acting on B2 receptors, bradykinin may play a beneficial, protective role in cardiovascular disease. Selective B2 agonists are available and have been shown to be effective in some animal models of human cardiovascular disease. These drugs may have potential for the treatment of hypertension and myocardial hypertrophy. 

Sugden, P. H. (1999). Signaling in myocardial hypertrophy Life after calcineurin Circ. Res. 84, 633-646. 

Akhtar SA, Luttrell RM, Rockman HA, Iaccarino G, Lefkowitz RJ, Joch WJ. 1998. Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy. Science 280 574-577. 

Laks MM, Morady F, Swan HJC.1973. Myocardial hypertrophy produced by chronic infusion of subhypertensive doses of norepinephrine in the dog. Chest 64 75-78. 

Nieto JL, Diaz-Laviade I, Gnillen A, Garcia-Barreno P, Haro A. 1993. Cardiac beta-adrenoceptors, G-proteins and adenylate cyclase regulation during myocardial hypertrophy. Cell Signal 5 169-179. 

Iaccarino, G., Dolber, P.C., Lefkowitz, R.J., and Koch, WJ. 1999. p-adrcncrgic receptor kinase-1 levels in catecholamine-induced myocardial hypertrophy regulation by P- but not cq-adrenergic stimulation. Hypertension 33 396-401. 

NO)-dependent process (Fruhbeck 1999). In this regard, NO production following leptin administration has been shown to be markedly depressed in obese animals (Beltowski et al. 2003). Interestingly, dietary-induced obesity in hypertensive rats results in slower recovery from stress-induced elevations in blood pressure and heart rate which was associated with myocardial hypertrophy and hyperleptinemia (Sedova et al. 2004). 

Myocardial hypertrophy The heart increases in size, and the chambers dilate. Initially, stretching of the heart muscle leads to a stronger contraction of the heart. However, excessive elongation of the fibers results in weaker contractions. This type of failure is termed systolic failure and is a result of a ventricle unable to pump effectively. Less commonly, patients with CHF may have diastolic dysfunction—a term applied when the ventricles ability to relax and accept blood is impaired by structural changes, such as hypertrophy. The thickening of the ventricular wall and subsequent decrease in ventricular volume decreases the ability of heart muscle to relax. In this case, the ventricle does not fill adequately, and the inadequacy of cardiac output is termed diastolic heart failure. 

This expectation is supported by other observations using the surrogate marker brain natriuretic peptide (BNP), a most sensitive indicator of myocardial hypertrophy and cardiac impairment [23], The expected curbing of cardiotoxicity in WBZ 4 anticancer therapy was confirmed by examining the mRNA levels of BNP in the left ventricle of mice from the same groups assayed for anticancer activity. The BNP mRNA levels were about 58% higher in the ventricles from imatinib-treated animals (Fig. 8.11b), while no significant difference was detected... 

Wu G, Toyokawa T, Hahn H, Dorn GW 2nd. Epsilon protein kinase C in pathological myocardial hypertrophy. Analysis by combined transgenic expression of translocation modifiers and Galphaq. J Biol Chem 2000 275 29,927-29,930. 

Hajri T, Ibrahimi A, Coburn CT, Knapp FF Jr, Kurtz T, Pravenec M, Abumrad NA (2001) Defective fatty acid uptake in the spontaneously hypertensive rat is a primary determinant of altered glucose metabolism, hyperinsulinemia, and myocardial hypertrophy. J Biol Chem 276 23661-23666... 

Several disorders can impair ventricular function and play a role in the development of DHF. DHF is seen often in patients with hypertension, coronary artery disease (CAD), valvular heart disease, and hypertrophic cardiomyopathies. Hypertension is the most common underlying cardiovascular disorder in patients with DHF. There are several proposed mechanisms by which hypertension may impair diastolic function. Hypertension can alter diastolic function through its effects on (1) wall tension, (2) myocardial hypertrophy and fibrosis, and (3) small vessel structure and function, and (4) by predisposing to epicardial CAD. An association between impaired LV filling and subnormal high-energy phosphate metabolism has been shown in hypertensive patients, even in the absence of left ventricular hypertrophy (LVH). ... 

Heart failure is due to defects in cardiac contractility (the vigor of heart muscle), leading to inadequate cardiac output. Signs and symptoms include decreased exercise tolerance and muscle fatigue, coupled with the results of compensatory responses (neural and humoral) evoked by decreases in mean BP. Increased SANS activity leads to tachycardia, increased arteriolar tone T afterload, 4- output, 4 renal perfusion), and increased venous tone (T preload, T fiber stretch). Activation of the renin-angiotensin system results in edema, dyspnea, and pulmonary congestion. Intrinsic compensation results in myocardial hypertrophy. These effects are summarized in Figure IH-4-1. 

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