Myocardial infarction secondary

In large series, sulprostone has had good tolerability with a very low complication rate. The most severe complication is myocardial infarction secondary to coronary spasm, with a frequency of one in 20 000, usually in smokers and women over 35 years of age with cardiovascular disease (SEDA-23, 436). 

RuDusky BM. Acute myocardial infarction secondary to coronary vasospasm during withdrawal from industrial nitroglycerin exposure—a case report. Angiology 2001 52(2) 143. ... 

Goldfischer JD (1960) Acute myocardial infarction secondary to ergot therapy Report of a case and review of the literature. New England Journal of Medicine 262 860-863. 

The primary endpoint was major adverse cardiovascular event (MACE), defined as cardiovascular death, stroke, or myocardial infarction. Secondary safety outcomes were cardiovascular death, stroke, myocardial infarction, all-cause death, serious myocardial ischemia, total myocardial ischemia. 

In another case, a 29-year-old man, who had at various times used Ma Huang, Xena-drine RFX, and Hydroxycut, had an acute myocardial infarction secondary to coronary artery aneurysms and thrombosis with the analogy of cocaine, the authors suggested that chronic use of ephedrine may have led to coronary artery aneurysms, perhaps due to recurrent vasospasm [74 ]. 

It is well accepted that hypertension is a multifactorial disease. Only about 10% of the hypertensive patients have secondary hypertension for which causes, ie, partial coarctation of the renal artery, pheochromacytoma, aldosteronism, hormonal imbalances, etc, are known. The hallmark of hypertension is an abnormally elevated total peripheral resistance. In most patients hypertension produces no serious symptoms particularly in the early phase of the disease. This is why hypertension is called a silent killer. However, prolonged suffering of high arterial blood pressure leads to end organ damage, causing stroke, myocardial infarction, and heart failure, etc. Adequate treatment of hypertension has been proven to decrease the incidence of cardiovascular morbidity and mortaUty and therefore prolong life (176—183). 

Ticlopidine inhibits the P2Yj2 platelet ADP receptor, thus inhibiting ADP-dependent activation of the GP Ilb/IIIa receptor. It has a slow onset of action and takes 3-7 days to reach its maximal antiplatelet effect. It is inactive in vitro and must undergo activation by the hepatic cytochrome p450 enzyme system. Secondary prevention trials have found that ticlopidine-treated patients have an estimated RRR of 33% for the composite endpoint of stroke, myocardial infarction, or vascular death after ischemic stroke. Significant adverse effects include bone marrow depression, rash, diarrhea, and thrombotic thrombocytopenic purpura. No clinical trials have studied ticlopidine for the treatment of stroke in the acute phase. 

Increased oxygen demand secondary to increased heart rates and blood pressure has been hypothesized to lead to myocardial infarction (especially in patients with fixed coronary disease) and/or ventricular arrhythmias. In patients with no history of cardiac disease, cocaine is thought to induce acute isehemie complications via vasospasm of the coronaries (Ascher et al. 1988). In addition, Virmani et al. (1988) have reported a 20 percent incidence of myocarditis thought to be secondary to accumulated microvascular injuries. 

Devise a pharmacotherapy and risk-factor modification treatment plan for secondary prevention of coronary heart disease events in a patient following myocardial infarction. 

As of 1995, almost 38% of all women 50 to 75 years of age were using HRT.1 It was in 1996 that the United States Preventive Services Task Force (USPSTF) first published its recommendations that not all postmenopausal women should be prescribed HRT, but rather, therapy should be individualized based on risk factors. This recommendation was further supported with publication of the Heart and Estrogen/Progestin Replacement Study (HERS) in 1998, which demonstrated that women who had established CHD were at an increased risk of experiencing a myocardial infarction within the first year of HRT use compared with a similar group of women without CHD risk factors. As a result, the authors concluded that HRT is not recommended for the secondary prevention of CHD.2 Then, in 2002, the Women s Health Initiative (WHI) report was published. This trial demonstrated that HRT was not protective against CHD but... 

The AHA/ASA guidelines recommend that antiplatelet therapy as the cornerstone of antithrombotic therapy for the secondary prevention of ischemic stroke and should be used in noncardioembolic strokes. Aspirin, dopidogrel, and extended-release dipyridamole plus aspirin are all considered first-line antiplatelet agents (see Table 13-1). The combination of aspirin and clopido-grel can only be recommended in patients with ischemic stroke and a recent history of myocardial infarction or coronary stent placement and then only with ultra-low-dose aspirin to minimize bleeding risk. 

Lipid modifying drugs (statins) have shown secondary cardio-vascular preventive effects (myocardial infarction) in a very large number of patients. Only one study (Shepherd et al. 2002) has been conducted in the elderly and showed similar results. However there was a significant increased cancer risk (25%). 

Chemical stimuli also underlie pain secondary to inflammation or ischemia (angina pectoris, myocardial infarction), or the intense pain that occurs during overdistention or spasmodic contraction of smooth muscle abdominal organs, and that may be maintained by local anoxemia developing in the area of spasm (visceral pain). 

Replacement therapy of hypothyroidism. Whether primary, i.e caused by thyroid disease, or secondary, i.e resulting from TSH deficiency, hypothyroidism is treated by oral administration of T4. Since too rapid activation of metabolism entails the hazard of cardiac overload (angina pectoris, myocardial infarction), therapy is usually started with low doses and gradually increased. The final maintenance dose required to restore a euthyroid state depends on individual needs (approx. 

Metoprolol is nsed in moderate hypertension, serions conditions of myocardial infarction, for preventing death of cardiovascular tissue, in angina, tachycardia, extrasystole, and for secondary prophylaxis after a heart attack. The most common synonyms are lopresor, betaloc, and others. 

European Secondary Prevention Study Group. Translation of clinical trials into practice a European population-based study of the use of thrombolysis for acute myocardial infarction. Lancet 1996 347(9010) 1203-7. 

Blockers are used as therapeutics in the treatment of hypertension, myocardial ischaemia (angina pectoris), tachyarrhythmias, and in the secondary prevention following myocardial infarction. More recently the cautious use of /3-blockers has been found to be of potential benefit in the treatment of congestive heart failure (NYHA stages II and III). 

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. 

Sulfinpyrazone is a uricosuric and also inhibits platelet functions, probably mainly as a result of some inhibition of prostaglandin synthesis. However clinical efficacy in secondary prevention of myocardial infarction is inconsistent at the most. 

The results of several large clinical trials using the statin drugs (discussed later) show that the tested drugs decreased the risk of both primary and secondary cardiovascular events. The incidence of myocardial infarction and death from cardiovascular disease was reduced in patients with hypercholesterolemia who never had a... 

Beta-adrenoceptor antagonists are used to treat hypertension, angina pectoris, arrhythmias and secondary myocardial infarct prevention following primary infarction (timolol, metoprolol and propranolol). 

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

Overview analyses have shown that low-dose aspirin reduces the secondary incidence of heart attack and stroke by about 25%. However, it elevates the low risk of serious gastrointestinal bleeding about twofold over placebo. Low-dose aspirin also reduces the incidence of first myocardial infarction. However, in this case, the benefit versus risk of gastrointestinal bleeding is less clear. The effects of aspirin on platelet function are discussed in greater detail in Chapter 34. 

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