Heart disease myocardial infarction

Sethi AA, Tybjaerg-Hansen A, Gron-holdt M-LM, Steffensen R, Schnohr P, Nordestgaard BG. Angiotensinogen mutations and risk for ischemic heart disease, myocardial infarction, and ischemic cerebrovascular disease. Ann Intern Med 2001 134 941-954. 

Angina, arrhythmias, congestive heart failure, ischemic heart disease, myocardial infarction Endocrine and metabolic... 

Decreased cardiac performance. Any number of factors that affect cardiac pumping ability may be responsible for initiating a change in myocardial performance. Factors such as ischemic heart disease, myocardial infarction, valve dysfunction, and hypertension may all compromise the heart s pumping ability.29 53 71 Also, cardiomyopathy may result from other diseases and infections.13... 

The natural history of the disease is determined by the onset and extent of chronic diabetic complications. Microangiopathic changes are diabetes-specific, causing retinopathy, nephropathy and alterations in the peripheral and autonomous nervous system. Macroangiopathy, which is more typical for Type-II diabetes, leads predominantly to cardiovascular complications with coronary heart disease, myocardial infarction and peripheral vascular occlusion. 

The root of Salvia miltiorrhiza has been used as Chinese folk medicine for the treatment of cardiovascular diseases, such as ischemia, angina pectoris, coronary heart disease, myocardial infarction, and hypertension. Many studies on the secondary metabolites from Salvia miltiorrhiza revealed that tanshinones were a group of compounds responsible for these biological activities, especially for the treatment of coronary artery disease and h5 rtension. 

Kinases which generate ATP can be assayed specifically, and creatine kinase, in view of its importance in the diagnosis of heart disease (myocardial infarction) has been much investigated and refined [103,104]. In principle any kinase generating or using ATP can be assayed and the method is among the most rapid and sensitive available. The reactions catalyzed by two kinases are shown ... 

Nitroglycerin remains the dmg of choice for treatment of angina pectoris. It has also been found useful for the treatment of congestive heart failure, myocardial infarction, peripheral vascular disease, such as Raynaud s disease, and mitral insufficiency, although the benefits of nitroglycerin in mitral insufficiency have been questioned. 

Age >40 yr, previous venous thromboembolism, chronic heart failure, acute respiratory failure, recent major surgery (within 2 wk), confined air/ground travel (>6 h duration within 1 wk of admission), inflammatory bowel disease, myocardial infarction, nephrotic syndrome, and ischemic stroke... 

Heart (angina, coronary artery disease, myocardial infarction, or heart failure)... 

Coronary artery disease Myocardial infarction Heart failure... 

Goal BP values are <140/90 for most patients, but <130/80 for patients with diabetes mellitus, significant chronic kidney disease, known coronary artery disease (myocardial infarction [MI], angina), noncoronary atherosclerotic vascular disease (ischemic stroke, transient ischemic attack, peripheral arterial disease [PAD], abdominal aortic aneurysm), or a 10% or greater Framingham 10-year risk of fatal coronary heart disease or nonfatal MI. Patients with LV dysfunction have a BP goal of <120/80 mm Hg. 

Cardiovascular disease Cardiomyopathy Congestive heart failure Myocardial infarction (heart attack)... 

Saito, K., Elce, J.S., Hamos, J.E., Nixon, R.A., 1993, Widespread activation of calcium-activated neutral proteinase (calpain) in the brain in Alzheimer disease a potential molecular basis for neuronal degeneration, Proc. Natl. Acad. Sci. U.S.A., 90, 2628—2632 Saido, T., Shibata, M., Takenawa, T., Murofushi, H., Suzuki, K., 1992, Positive regulation of p-calpain action by polyphosphoinositides, J. Biol. Chem., 267, 24585—24590 Sandmann, S., Yu, M., Unger, T., 2001, Transcriptional and translational regulation of calpain in the rat heart after myocardial infarction - effects of AT( 1) and AT(2) receptor antagonists and ACE inhibitor, Br. J. Pharmacol. 132, 767-777... 

Cardiovascular disease Coronary artery disease Congestive heart failure Myocardial infarction Neurologic disorders Alzheimer s disease Epilepsy... 

Although betaxolol generally elicits less systemic beta-blockade than do noncardioselective agents, it does cause undesirable systemic effects in some patients. Reported adverse experiences include congestive heart failure, myocardial infarction, respiratory difficulties strongly suggestive of obstructive airway disease, weakness with severe sinus bradycardia, and wheezing with objective reduction in pulmonary function. 

The plaques of Alzheimer s disease and the fibrous state of the prions of mad cow disease (both with resulting brain destruction), the thrombi of stroke (cerebral thrombosis) and of heart attack (myocardial infarction), and the familiar manifestation of death (rigor mortis) represent excursions too far in the direction of protein insolubility. The favorable actions of antioxidants keep proteins from becoming so soluble (unfolded) that protein function disappears and proteolytic degradation ensues. Of course, the lack of blood clotting, hemophilia (the lack of clotting proteins to become insoluble by association of oil-like domains), results in death. Such devastations result from loss of proper balance between solubility and insolubility. They represent excursions too far from the cusp of insolubility, that is, too far from the boundary between insolubility and solubility. 

Oxidative stress is defined as an imbalance between the systemic manifestation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and a biological system s ability to readily detoxify the reactive intermediates (Sies, 2015). It results in cellular damage linked to the atherosclerosis, hypertension, heart failure, myocardial infarction, malignancy, and neurodegenerative diseases such as Parkinson s disease, Alzheimer s disease, and ALS (Figure 3.8). 

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. 

Another example is the use of Tc-sestamibi, approved for use in the evaluation of coronary artery disease and myocardial infarction, in patients with breast cancer. Use in breast cancer is under investigation by a number of physicians. The data are not yet sufficient to determine the efficacy of this agent in this setting. Its safety, of course, has already been demonstrated as part of its initial evaluation for heart disease. 

There can be a number of underlying causes of CHE. The most prevalent is the lack of oxygenated blood reaching the heart muscle itself because of coronary artery disease with myocardial infarction (111). Hypertension and valvular disease can contribute to CHE as well, but to a lesser extent in terms of principal causes for the disease. 

Other Cardiovascular Agents Effecting Atherosclerosis. A large amount of clinical data is available concerning semm Upid profiles in patients subjected to dmg therapy for other cardiovascular diseases. Atheroma, for example, may be the underlying cause of hypertension and myocardial infarction. There are on the order of 1.5 million heart attacks pet year in the United States (155). 

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). 

A third study (85) enrolled 7825 hypertensive patients (55% males and 45% females) having diastoHc blood pressures (DBP) of 99—104 mm Hg (13—14 Pa) there were no placebo controls. Forty-six percent of the patients were assigned to SC antihypertensive dmg therapy, ie, step 1, chlorthaUdone step 2, reserpine [50-55-5] or methyldopa [555-30-6], and step 3, hydralazine [86-54-4]. Fifty-four percent of the patients were assigned to the usual care (UC) sources in the community. Significant reductions in DBP and in cardiovascular and noncardiovascular deaths were noted in both groups. In the SC group, deaths from ischemic heart disease increased 9%, and deaths from coronary heart disease (CHD) and acute myocardial infarctions were reduced 20 and 46%, respectively. 

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