Myocardial infarction and

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

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). 

Antiplatetelet Trialists Collaboration (2002) Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 324 71-86... 

Thromboembolic events (myocardial infarction and stroke, see below)... 

Other contraindications for die anticholinergics include tachyarrhythmias, myocardial infarction, and congestive heart failure (unless bradycardia is present). 

Adverse reactions include transitory stinging on initial instillation, blurring of vision, mydriasis, increased redness, irritation, discomfort, and increased IOP. Systemic adverse reactions include headache, browache, palpitations, tachycardia, arrhythmias, hypertension, myocardial infarction, and stroke. 

An estimated oral dose of 260 mg endosulfan/kg caused severe seizures in a 43-year-old man, and brain death from cerebral herniation and massive cerebral edema occurred within 4 days of exposure (Boereboom et al. 1998) there were no signs of myocardial infarction and only slight congestion of the heart, but pulmonary congestion and atelectasis were evident at autopsy. 

CR is distributed in various organs with highest concentrations in skeletal muscle, myocardium, and brain and lesser amounts in the gastrointestinal tract, uterus, urinary bladder, and kidney ( ). The CR content of liver and red blood cells is negligible so that diseases of these tissues are unlikely to increase the serum CR activity. The serum CR level begins to increase in 2-4 hours after myocardial infarction and reaches a peak in 24-36 hours and returns to normal in about 3 days. 

Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to improve vascular outcomes due to their cholesterol-lowering effects as well as multiple pleiotropic effects. In high-risk populations, statin therapy is known to reduce the risk of vascular events such as myocardial infarction and stroke. A meta-analysis of 10 trials involving 79,494 subjects showed that statin therapy reduced the incidence of stroke by 18%, major coronary events by 27%, and all-cause mortality by 15%. The SPARCL trial recently showed that high-dose HMG-CoA reductase inhibitors prevent recurrent stroke and transient ischemic attacks. ... 

Antiplatelet Trialist Collaboration. Collaborative overview of randomised trials of antiplatelet treatment. Part I prevention of death, myocardial infarction and stroke by prolonged antiplatelet therapy in various categories of patients. BMJ 1994 308 81-106. 

Gent M. A systematic overview of randomised trials of antiplatelet agents for the prevention of stroke, myocardial infarction and vascular death. In Hass WK, Easton ID, editors. Ticlo-pidine, platelets and vascular disease. New York Springer-Verlag 1993 p99-116. 

Komrad MS, Coffey CE, Coffey KS, McKinnis R, Massey EW, Califf RM. Myocardial infarction and stroke. Neurology 1984 34 1403-1409. 

Carotenoids and cardiovascular diseases — Numerous epidemiological studies aimed to study the relationship of carotenoids and cardiovascular diseases (CVDs) including coronary accident risk and stroke. It appeared then that observational studies, namely prospective and case-control studies, pointed to a protective effect of carotenoids on myocardial infarct and stroke, but also on some atherosclerosis markers such as intima media thickness (IMT) of the common carotid artery (CCA) and atheromatous plaque formation. 

Among 27 prospective and case-control studies, 16 reported inverse associations between some carotenoids and CVDs, taking plasma or serum concentration as carotenoid biomarkers (11 of 16 studies), dietary intake (5 of 16 studies), or adipose tissue level (1 of 16 studies). With regard to the findings from the studies based on CVD risk, only two of seven presented significant inverse associations of carotenoids, particularly lycopene and P-carotene, whereas five studies of nine showed inverse correlations between myocardial infarcts and lycopene and/or P-carotene the others presented no associations. ... 

Some prospective and case-control studies also investigated the relationship of carotenoids and the evolution of CCA-IMT. Although the EVA study showed no association between total carotenoids and IMT, others like the ARIC study, the Los Angeles Atherosclerosis Study, " and the Kuopio Ischaemic Heart Disease Risk Factor Study demonstrated the protective role of isolated carotenoids such as lycopene, lutein, zeaxanthin, and P-cryptoxanthin on IMT. Thus, findings from prospective and case-control studies have suggested that some carotenoids such as lycopene and P-carotene may present protective effects against CVD and particularly myocardial infarcts and intima media thickness, a marker of atherosclerosis. 

Kardinaal, A.E. et al.. Association between beta-carotene and acute myocardial infarction depends on polyunsaturated fatty acid status the EURAMIC study (European Study on Antioxidants, Myocardial Infarction, and Cancer of the Breast), Arterioscler. Thromb. Vase. Biol, 15, 726, 1995. 

O Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that is most often due to coronary atherosclerosis. Common clinical manifestations of ischemic heart disease include chronic stable angina and the acute coronary syndromes of unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. 

List the quality indicators of care for myocardial infarction and explain the rationale behind each indicator. 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

Symptoms may be confused for a myocardial infarction and objective testing must be performed to establish the diagnosis. 

The speed and appropriateness of therapy administered in the initial hours after sepsis develops influences outcome, as is the case for acute myocardial infarction and cerebrovascular accidents.22... 

Acute coronary syndromes Ischemic chest discomfort at rest, most often accompanied by ST-segment elevation, ST-segment depression, or T-wave inversion on the 12-lead electrocardiogram. Furthermore, it is caused by plaque rupture and partial or complete occlusion of the coronary artery by thrombus. Acute coronary syndromes include myocardial infarction and unstable angina. Former terms used to describe types of acute coronary syndromes include Q-wave myocardial infarction, non-Q-wave myocardial infarction, and unstable angina. 

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