Myocardial infarction and coronary artery

WlNKELMANN BR, NAUCK M, KlEIN B, Russ AP, Bohm BO, Siekmeier R, Ihn-ken K, Verho M, Gross W, Marz W. Deletion polymorphism of the angiotensin I-converting enzyme gene Is associated with increased plasma angiotensin-con-verting enzyme activity but not with increased risk for myocardial infarction and coronary artery disease. Ann Intern Med 1996 125 19-25. 

The above findings confirm that exposure to PSCI RCAs by airborne dispersion or by contamination in solution produce abrupt and marked increases in SBP and DBP, with resolution within about 0.5 h of the start of exposure. The magnitude and duration of the changes can be tolerated without significant medical hazards in healthy individuals. However, as with other stressful situations, some susceptible individuals may be at increased risk from the induced transient hypertensive episode this will include those with essential hypertension, established myocardial infarction and coronary artery disease, cardiac arrhythmias and arterial aneurysms (Ballantyne, 1977a, 1987 Ballantyne and Salem, 2004). 

Da Silva B, Tschampa J, Beron J, Fredrick L, Patwardhan M, Zachry W, et al. Evaluation of myocardial infarction and coronary artery disease in subjects taking lopinavir/ritonavir a study using clinical trial and pharmacovigilance databases. Int J Clin Pharmacol Ther 2012 50(6) 391-402. 

YuXC et al. (2001) Cardiac effects of the extract and active components of Radix stephaniae tetrandrae II. Myocardial infarct, arrhythmias, coronary arterial flow and heart rate in the isolated perfused rat heart. Life Sci 68(25) 2863-2872... 

Gensini GF, Fusi C, Conti AA et al. Cardiac troponin I and Q-wave perioperative myocardial infarction after coronary artery bypass surgery. Crit Care Med 1998 26 1986. 

Many clinical trials designed to show a difference between the two drugs must be very large for example, studies to improve mortality and morbidity after myocardial infarction or coronary artery bypass surgery involve tens of thousands of study subjects. These are major undertakings... 

BRADYKININ AND THE EEFECTS OE ACE INHIBITORS ACE inhibitors are used widely in the treatment of hypertension, and they reduce mortality in patients with diabetic nephropathy, left ventricular dysfunction, previous myocardial infarction, or coronary artery disease. ACE inhibitors block the conversion of Angl to Angll, a potent vasoconstrictor and growth promoter (Figure 24-2) (see Chapter 30). Studies using the specific bradykinin B antagonist HOE-140 demonstrate that bradykinin also contributes to many of the protective effects of ACE inhibitors. The contribution of bradykinin to the effects of ACE inhibitors may result not only from decreased degradation of bradykinin but also from induction of enhanced receptor sensitivity. 

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. 

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. 

Acute MI (myocardial infarction), 5 107 antianginal agents for, 5 110t and coronary arterial thrombosis, 5 170 Acute myelogenous leukemia (AML), and benzene exposure, 3 616 Acute oral toxicity... 

G2I. Graziani, M. S., Zanolla, L., Righetti, G., Nicoli, M., Modena, N., Dimitri, G., Menegatti, G.. and Vassanelli, C., Lipoprotein(a) concentrations are increased in patients with myocardial infarction and angiographically normal coronary arteries. Eur. J. Clin. Chem. Clin. Biochem. 31, 135-137 (1993). 

Cardiovascular Effects. Myocardial infarction, severe coronary luminal narrowing, and internal alteration of the carotid artery were found in two patients injected 21 -30 years before with an unreported amount of Thorotrast (Isner et al. 1978). The authors concluded that the vascular effects were the result of chronic alpha irradiation. The patients were injected in the carotid artery, and thorotrastoma (see Other Systemic Effects, below) was found in both patients. 

Following intravenous injection of Thorotrast, cirrhosis of the liver was the primary systemic effect in humans and animals. Hematological disorders (aplastic anemia, leukemia, myelofibrosis, and splenic cirrhosis), cardiovascular effects (myocardial infarction, severe coronary luminal narrowing and internal alteration of the carotid artery), and Thorotrastoma (localized fibrosis surrounding deposits of Thorotrast) were also found in patients injected with Thorotrast. The effects of Thorotrast were a result of the radiological toxicity of thorium. 

CASS Principal Investigators and their Associates. Myocardial infarction and mortality in the Coronary Artery Surgery Study. N Engl J Med 1984 310 750. 

Highly recommended are jS-blockers for those who have a prior MI event. They showed a significant effect on death. Recent studies suggest that patients who have coronary artery disease without acute myocardial infarction and/or congestive heart failure have approximately the same protective benefit against death. 

Dobutamine is widely used to increase myocardial contractility, cardiac output, and stroke volume in the peri-operative period. It is less likely to increase heart rate than dopamine. There is evidence that dobutamine can increase both myocardial contractility and coronary blood flow. This makes it particularly suitable for use in patients with acute myocardial infarction. Dobutamine is also suitable for treating septic shock associated with increased filling pressures and impaired ventricular function. Owing to the competing a and 3 activity there is usually little change in mean arterial pressure. 

Aspirin decreases the incidence of transient ischemic attacks, unstable angina, coronary artery thrombosis with myocardial infarction, and thrombosis after coronary artery bypass grafting (see Chapter 34). 

A day after a dose of intravenous methylprednisolone 60 mg a 79-year-old woman developed acute thoracic pain and collapsed. An electrocardiogram showed signs of a myocardial infarction and her cardiac enzyme activities were raised. She died within several hours. Autopsy showed an anterior transmural myocardial infarction and mild atheromatous lesions in the coronary arteries. 

In 12 patients with type 2 diabetes, a combination of nateglinide 120 mg or placebo with metformin 500 mg before each meal on two separate days was well tolerated (19). One patient taking nateglinide had a headache. One patient was withdrawn because of a myocardial infarction and had multi-vessel coronary artery disease on catheterization. 

One patient taking nateglinide had a headache. One patient was withdrawn because of a myocardial infarction and had multivessel coronary artery disease on catheterization. 

Tissue plasminogen activator has been used successfully to treat acute myocardial infarction, and the benefits of this treatment are well documented.102,116 This drug, however, does not seem to be superior to other thrombolytics when treating coronary artery thrombosis, and streptokinase may be a more cost-effective method of treating myocardial infarction. Alternatively, t-PA may be more effective than other thrombolytics in its ability to initially reopen cerebral vessels this drug is often used preferentially during ischemic stroke.4,44 Hence, the added cost of t-PA may be justified in this situation. 

Eichner JE, Kuller LH, Orchard TJ, Grandits GA, McCallum LM, Ferrell RE, Neaton JD. Relation of apolipoprotein E phenotype to myocardial infarction and mortality from coronary artery disease. Am. J. Cardiol. 1993 71 160-165. 

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