Myocardial infarction, treatment inhibitors

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. 

High risk Has unstable or symptomatic angina, despite treatment Has poorly controlled hypertension Has severe congestive heart failure (NYHA Class III or IV) Had a recent myocardial infarction or stroke within the past 2 weeks Has moderate or severe valvular heart disease Phosphodiesterase inhibitor is contraindicated... 

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. 

Arterial thrombi (white thrombi) are formed initially from both platelets and fibrin in medium-sized arteries on the basis of atherosclerosis. These thrombi can lead to symptoms of, among others, myocardial ischemia and myocardial infarction. The treatment is primarily aimed at prevention of thrombus formation with platelet aggregation inhibitors. For the treatment of myocardial infarction thrombolytic agents are used and for secondary prevention both oral anticoagulants and anti-platelet drugs are employed. 

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. 

Captopril, as well as other ACE inhibitors, is indicated in the treatment of hypertension, congestive heart failure, left ventricular dysfunction after a myocardial infarction, and diabetic nephropathy. In the treatment of essential hypertension, captopril is considered first-choice therapy, either alone or in combination with a thiazide diuretic. Decreases in blood pressure are primarily attributed to decreased total peripheral resistance or afterload. An advantage of combining captopril therapy with a conventional thiazide diuretic is that the thiazide-induced hypokalemia is minimized in the presence of ACE inhibition, since there is a marked decrease in angiotensin Il-induced aldosterone release. 

ACE inhibitors have a particularly useful role in treating patients with chronic kidney disease because they diminish proteinuria and stabilize renal function (even in the absence of lowering of blood pressure). This effect is particularly valuable in diabetes, and these drugs are now recommended in diabetes even in the absence of hypertension. These benefits probably result from improved intrarenal hemodynamics, with decreased glomerular efferent arteriolar resistance and a resulting reduction of intraglomerular capillary pressure. ACE inhibitors have also proved to be extremely useful in the treatment of heart failure, and after myocardial infarction, and there is recent evidence that ACE inhibitors reduce the incidence of diabetes in patients with high cardiovascular risk (see Chapter 13). 

An important class of orally active ACE inhibitors, directed against the active site of ACE, is now extensively used. Captopril and enalapril are examples of the many potent ACE inhibitors that are available. These drugs differ in their structure and pharmacokinetics, but in clinical use, they are interchangeable. ACE inhibitors decrease systemic vascular resistance without increasing heart rate, and they promote natriuresis. As described in Chapters 11 and 13, they are effective in the treatment of hypertension, decrease morbidity and mortality in heart failure and left ventricular dysfunction after myocardial infarction, and delay the progression of diabetic nephropathy. 

Adverse effects The adverse effects include hypotension, worsening renal function, and hyperkalemia. The ACE inhibitors should remain the first-choice treatment in patients after complicated acute myocardial infarction. 

The main argument in favor of a beneficial effect of ACE inhibition on coronary heart diseases comes from the pooled results of the SOLVE) treatment trial, the SOLVE) prevention trial, and the SAVE, AIRE, and TRACE studies, which indicate a 21% (95% Cl, 11-29%, p <. 001) relative risk reduction for myocardial infarction associated with ACE inhibitor therapy. Enalapril (SOLVE)) significantly reduced hospitalization for unstable angina, and captopril (SAVE) reduced revascularization procedures (291). In patients treated for 38 to 42 months with enalapril or captopril and selected on the basis of a reduction in ejection fraction with or without heart failure, it is necessary to treat 49 patients to avoid one myocardial infarction (95% Cl 32-117). 

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