Myocardial dysfunction, effect

Cardiovascular effects Limit use of levorphanol in acute Ml or in cardiac patients with myocardial dysfunction or coronary insufficiency because the effects of levorphanol on the heart are unknown. 

Methoxyflurane (Penthmne) is the most potent inhala-tional agent available, but its high solubility in tissues limits its use as an induction anesthetic. Its pharmacological properties are similar to those of halothane with some notable exceptions. For example, since methoxyflurane does not depress cardiovascular reflexes, its direct myocardial depressant effect is partially offset by reflex tachycardia, so arterial blood pressure is better maintained. Also, the oxidative metabolism of methoxyflurane results in the production of oxalic acid and fluoride concentrations that approach the threshold of causing renal tubular dysfunction. Concern for nephrotoxicity has greatly restricted the use of methoxyflurane. 

Cardiovascular disease. The hypotensive effects of thiopentone are exaggerated in patients with myocardial dysfunction, fixed cardiac output (valvular stenosis, constrictive pericarditis), and in the hypovolaemic... 

In acute or chronic ischemia patients, angiogenic potential of transplanted cells is of the greatest importance. The patients with chronic nonviable scar and myocardial dysfunction are more likely to benefit from the cells that, either directly or indirectly (via paracrine effect) (47), improve the contractility of the treated myocardium (9). Autologous skeletal myoblasts have been successfully expanded in vitro and implanted in the myocardia of animals. Although they do not contract synchronously with the rest of the myocardium and do not integrate into it, they have been shown to improve contractility... 

C. Pantos, I. Mourouzis, S. Tzeis, P. Moraitis, V. Malliopoulou, D.D. Cokkinos, H. Carageorgiou, D. Varonos, D.V. Cokkinos, Dobutamine administration exacerbates postischemic myocardial dysfunction in isolated rat hearts An effect reversed by thyroxine pre-treatment, Eur J Pharmacol 460,155-161 (2003). 

In patients with elevated systemic vascular resistance and normal-to-elevated systemic blood pressure, afterload reduction with nitroprusside is logical it should be emphasized that nitroprus-side also increases venous capacitance, thereby also decreasing preload. In the context of myocardial dysfunction, afterload reduction will typically lead to improved forward cardiac output. Nitroprusside may also be effective when the systemic vascular resistance is elevated and systemic blood pressure is reduced the caveat in this more complex hemodynamic setting is that the load reduction produced by nitroprusside must be counterbalanced by an increase in stroke volume. This derivative increase in stroke volume may not occur in the patient with advanced heart failure rather, the result will be a further reduction in mean arterial pressure and the potential risk of peripheral organ hypoperfusion. An alternative approach would be the use of an inotropic-dilator drug such as milrinone, which will provide both preload and afterload reduction its concurrent positive inotropic effect may offset the reduction in mean arterial pressure that can occur from vasodilation alone. 

It is not easy to demonstrate the direct effect of free radicals on myocardial tissue. McCord and Frido-viCH (1969) designed an experiment that involved the electrolytic generation of the O2 " radical. Jack-son et al. (1986) used electrolysis of the perfusion medium to study free radicals mediated tissue injury. Stewart etal. (1988) and Chahine etal. (1991) observed myocardial dysfunction in isolated perfused rabbit and rat hearts subjected to electrolysis. Lecour et al. (1998) suggested that both hydroxyl and superoxide radicals were formed during electrolysis. 

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... 

Blood pressure lowering drugs reduce risk of stroke (and myocardial infarction and death) in middle aged patients and even better in the elderly (NNT 86 vs 29 over 5 years) (Pearce 1998). However in the elderly the dysfunction in the autoregulation of brain blood flow, salt and fluids, and increased sensitivity to adverse effects and symptoms may change the picture. 

Heart failure Some ACEIs are effective in the management of CHF, usually as adjunctive therapy and in patients who demonstrate clinical signs of CHF or have evidence of left ventricular systolic dysfunction within the first few days after an acute myocardial infarction (Ml). 

Sinusas AJ, Watson DD, Cannon JM, Jr., Beller GA. Effect of ischemia and postischemic dysfunction on myocardial uptake of technetium-99m-labeled... 

Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction EMIAT. European myocardial infarct amiodarone trial investigators. Lancet. Mar 8 1997 349(9053) 667-674. 

The piperidines, e.g. thioridazine, pipothiazine and pericyazine, have the lowest potential to cause extrapyramidal effects. Thioridazine is one of the most sedative phenothiazines. It may decrease the inotropic activity of digitalis by its quinidine-like action, which can cause myocardial depression, decreased efficiency of repolarization, and increased risk of tachyarrhythmias. With thioridazine drug induced sexual dysfunction and especially cardiotox-icity with prolongation of the QT-interval are more frequently seen than with other phenothiazines. For the above reasons thioridazine is withdrawn from the market in many countries. 

Low-dose diuretics and /3-blockers, which have demonstrated positive effects on mortality, are indicated as first choice treatment. This is still maintained in the new recommendations for patients with uncomplicated hypertension (Table 5). However, other treatments are recommended for hypertensive patients with associated diseases (Table 6). Hypertension with diabetes or renal dysfunction must be treated with an ACE inhibitor in the first instance. Patients with myocardial infarction should be treated with /S-blockers and in specific cases with an ACE inhibitors. For patients with heart failure, the treatment of choice is an ACE inhibitor and diuretics. For older patients with isolated SBP, low-dose diuretics are recommended as the first step treatment and some of the CCB with long acting profile can be considered an alternative treatment. 

Infrequent reactions to interferon therapy include proteinuria, renal toxicity, autoimmune disease, thyroid disease, ophthalmic toxicity, pulmonary dysfunction (pulmonary infiltrates, pneumonitis, and pneumonia), and cardiovascular effects (tachycardia, arrhythmia, hypotension, cardiomyopathy, and myocardial infarction). Rarely, the body may develop antibodies against interferons that inhibit their effectiveness. 

Diuretics are the mainstay of heart failure management and are discussed in detail in Chapter 15. They have no direct effect on cardiac contractility their major mechanism of action in heart failure is to reduce venous pressure and ventricular preload. This results in reduction of salt and water retention and edema and its symptoms. The reduction of cardiac size, which leads to improved pump efficiency, is of major importance in systolic failure. Spironolactone and eplerenone, the aldosterone antagonist diuretics (see Chapter 15), have the additional benefit of decreasing morbidity and mortality in patients with severe heart failure who are also receiving ACE inhibitors and other standard therapy. One possible mechanism for this benefit lies in accumulating evidence that aldosterone may also cause myocardial and vascular fibrosis and baroreceptor dysfunction in addition to its renal effects. 

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