java barcode reader api Coronary Artery & Other Vascular Abnormalities in Objective-C

Generation QR-Code in Objective-C Coronary Artery & Other Vascular Abnormalities

2 Coronary Artery & Other Vascular Abnormalities
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There have been a number of reports of myocardial infarction during pregnancy It is known that pregnancy predisposes to dissection of the aorta and other arteries, perhaps because of the accompanying connective tissue changes The risk may be particularly high in patients with Marfan or Ehlers-Danlos syndromes However, coronary artery dissection is responsible for only a minority of the infarctions; most are caused by atherosclerotic CAD or coronary emboli Most of the events occur near term or shortly following delivery, and paradoxical emboli through a PFO has been implicated in some cases Clinical management is essentially similar to that of other patients with acute infarction, unless there is a connective tissue disorder If nonatherosclerotic dissection is present, coronary intervention is risky as further dissection can be aggravated In most instances, conservative management is warranted
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deaths occurring during athletic participation is unknown, but estimates at the high school level range from one in 300,000 to one in 100,000 participants Death rates among more mature athletes increase as the prevalence of CAD rises These numbers highlight the problem of how to screen individual participants Even an inexpensive test such as an ECG would generate an enormous cost if required of all athletes, and it is likely that few atrisk individuals would be detected Echocardiography, either as a routine test or as a follow-up examination for abnormal ECGs, would be prohibitively expensive except for the elite professional athlete Thus, the most feasible approach is that of a careful medical history and cardiac examination performed by personnel aware of the conditions responsible for most sudden deaths in competitive athletes In a series of 158 athletic deaths in the United States between 1985 and 1995, hypertrophic cardiomyopathy (36%) and coronary anomalies (19%) were by far the most frequent underlying conditions LV hypertrophy was present in another 10%, ruptured aorta (presumably due to Marfan syndrome or cystic medial necrosis) in 6%, myocarditis or dilated cardiomyopathy in 6%, aortic stenosis in 4%, and arrhythmogenic RV dysplasia in 3% In addition, commotio cordis, or sudden death due to direct myocardial injury, may occur More common in children, it may occur even after a minor direct blow to the heart; it is thought to be due to the precipitation of a premature ventricular contraction just prior to the peak of the T wave on ECG It is likely that a careful family and medical history and cardiovascular examination will identify some individuals at risk A family history of premature sudden death or cardiovascular disease or of any of these predisposing conditions should mandate further workup, including an ECG and echocardiogram Symptoms of chest pain, syncope, or nearsyncope also warrant further evaluation A Marfan-like appearance, significant elevation of BP or abnormalities of heart rate or rhythm, and pathologic heart murmurs or heart sounds should also be investigated before clearance for athletic participation is given Such an evaluation is recommended before participation at the high school and college levels and every 2 years during athletic competition Stress-induced syncope or chest pressure may be the first clue to an anomalous origin of a coronary artery Anatomically, this lesion occurs most often when the left anterior descending artery arises from the right coronary cusp and traverses between the aorta and pulmonary trunks The slit-like orifice that results from the angulation at the vessel origin is thought to cause ischemia when the aorta and pulmonary arteries enlarge during rigorous exercise The toughest distinction may be in sorting out the healthy athlete with LVH from the athlete with hypertrophic cardiomyopathy In general, the healthy athlete s heart is less likely to have an unusual pattern of LVH, LA enlargement, an abnormal ECG, an LV cavity < 45 mm in diameter at end-diastole, an abnormal diastolic filling pattern, a family history of hypertrophic cardiomyopathy, and the athlete is more likely to be male than the individual with hypertrophic cardiomyopathy
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