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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term low-flow oxygen therapy can lead to improved exercise capacity and improved hemodynamics in selected patients with pulmonary hypertension. We report a patient who presented with severe exercise limitation and anginal chest pain that appeared to result from pulmonary hypertension and predominantly right ventricular ischemia. Acute oxygen therapy led to relief of pain but no change in exercise capacity or of pulmonary hypertension. After eight months of oxygen therapy, the patient's pulmonary hypertension was unchanged, but right ventricular hypertrophy and marked increases in exercise cardiac output and exercise capacity developed. Thus, oxygen can relieve right ventricular angina and facilitate the development of compensatory hypertrophy.
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PMID:Relief of right ventricular angina and increased exercise capacity with long-term oxygen therapy. 183 Aug 39

Hypertension is a major contributor to cardiovascular morbidity and mortality, increasing risk threefold. It predisposes to every clinical manifestation of coronary heart disease, now the most common and lethal outcome. It is as relevant a risk factor in the elderly as in the young. Risk is proportional to the degree of blood pressure elevation without a discernible critical value. Cardiovascular sequelae do not derive chiefly from the diastolic component, and isolated systolic hypertension confers increased risk at all ages. Hypertension tends to cluster with other cardiovascular risk factors, which must be taken into account in evaluating the risk and in choosing treatment. The excess cardiovascular risk in hypertension is concentrated in those with an increased total/high density lipoprotein cholesterol ratio, glucose intolerance, cigarette smoking, elevated fibrinogen, and electrocardiogram abnormalities. Left ventricular hypertrophy (LVH) is a common feature of hypertension and an ominous harbinger of cardiovascular sequellae. Electrocardiographic evidence of LVH, when manifested by repolarization abnormalities and voltage elevations, is particularly hazardous, reflecting not only anatomical hypertrophy but also ischemia. Electrocardiogram-LVH adds to cardiovascular risk associated with X ray or echocardiographic evidence of anatomical LVH. Because of a tendency to ventricular ectopy, LVH is associated with increased risk of sudden death. Electrocardiogram-LVH can be corrected or avoided by control of hypertension and weight reduction. The efficacy of correcting LVH remains to be demonstrated but benefits seem likely.
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PMID:Hypertension, hypertrophy, and the occurrence of cardiovascular disease. 183 77

Epidemiological data has established a relationship between left ventricular hypertrophy (LVH) and sudden cardiac death. This relationship is independent. The search for ventricular and atrial arrhythmias in hypertensives confirms a greater prevalence of these arrhythmias in patients with LVH. The mechanism of these arrhythmias is multifactorial: ischemia, subendocardial fibrosis, increased sympathetic tone, electrolyte disturbances, age, and hemodynamic changes may be arrhythmogenic substrates both at the ventricular and auricular levels. The relationship between LVH (marker or cause) and the detected arrhythmias remain obscure. The most sensitive markers of severity seem to be the ECG parameters (LVH with overload), echocardiographic mass (greater than + 20%) and septal thickness (greater than 12 mm). The evolution of arrhythmias with regression of LVH is unknown. Respect of electrolyte equilibrium would seem to be the only unquestioned therapeutic intervention.
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PMID:[Left ventricular hypertrophy and arrhythmia. An aspect of hypertensive cardiomyopathy]. 183 64

The effects of regression of left ventricular hypertrophy following atenolol and bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats (SHR) were studied. Atenolol (50 mg/kg/day) and bunazosin (5 mg/kg/day) were administered to SHR from 19 to 26 weeks of age, whereas tap water was given to control SHR and normotensive Wistar-Kyoto rats (WKY). Both atenolol and bunazosin significantly decreased arterial blood pressure and significantly decelerated the increase in left ventricular weight in SHR. At the end of the long-term treatment, hearts were removed and perfused by the working heart technique for 15 min, and then global ischemia was induced for either 10 or 30 min. The ischemic heart was reperfused for 30 min. The pressure-rate product and the extent of recovery of the coronary flow after reperfusion following 30 min of ischemia in the bunazosin-treated SHR were significantly higher than those in the control SHR and the atenolol-treated SHR. The levels of adenosine triphosphate (ATP), creatine phosphate (CrP), and energy charge potential in the SHR heart reperfused after 30 min of ischemia were significantly lower than those in the reperfused WKY. Both atenolol and bunazosin improved the restoration of ATP and CrP in SHR after reperfusion following 30 min of ischemia. In conclusion, antihypertensive therapy with either atenolol or bunazosin was effective in preventing cardiac hypertrophy and ischemic damage caused by different mechanisms. Factors resulting from stimulation of the cardiac alpha 1 adrenoceptor may play an important role in the development of hypertensive cardiac hypertrophy, just as factors resulting from stimulation of the beta 1-adrenoceptor do.
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PMID:Effects of regression of left ventricular hypertrophy following atenolol or bunazosin therapy on ischemic cardiac function and myocardial metabolism in spontaneously hypertensive rats. 183 20

Changes in left ventricular remodeling due to antihypertensive therapy have been demonstrated in experimental animal studies although no quantitative relationship has been shown between correction of blood pressure and regression of myocardial mass. As regards the qualitative aspects of regression, only the ACE inhibitors have been shown to prevent the development and induce regression of the excess collagen content of the myocardium submitted to chronic pressure overload. The problems posed by remodeling in clinical practice are more complex: should regression of myocardial mass itself be the therapeutic objective in the absence of a practical method of analysing the interstitial factor of hypertensive disease or should we concentrate on the satellite problems of hypertrophy which are correction of ischemia, left ventricular filling abnormalities and arrhythmias. For each of these clinical problems, the benefits attributed to changes in remodeling, though probable, are to a large degree hypothetical. The benefits offered by these drugs which reduce ventricular hypertrophy are, however, considerable.
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PMID:[Left ventricular remodeling and hypertension. Course with antihypertensive therapy]. 183 22

Although left ventricular hypertrophy is an adaptative mechanism to increased load, its development represents a pathological state which can affect patients' health in many ways. Systemic hypertension is often associated to left ventricular hypertrophy; a correlation exists between ambulatory blood pressure monitoring daytime mean blood pressure values and left ventricular mass. Left ventricular hypertrophy is an independent risk factor for cardiovascular events, and the pattern of concentric left ventricular hypertrophy is associated with higher morbidity and mortality. The mechanism by which left ventricular hypertrophy impair life expectancy is not completely known; arrhythmias and ischemia may often develop in patients with secondary left ventricular hypertrophy and can contribute to worsen prognosis. Left ventricular mechanics is also affected by hypertrophy. Systolic function is usually normal at rest, but its response to exercise can be blunted when hypertrophy develops. Diastolic dysfunction is often present in patients with hypertension, even before left ventricular hypertrophy occurs, and it can impair systolic function by hampering filling resulting mostly in an impairment in the adjustment to exercise. Effective antihypertensive therapy leads to a decrease in left ventricular hypertrophy and an improvement in diastolic mechanics.
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PMID:[Ventricular hypertrophy as an expression of hypertensive damage]. 184 9

In order to assess myocardial perfusion in patients with Friedreich's ataxia, we carried out dipyridamole-thallium imaging in 13 cardiologically asymptomatic patients (aged 16 to 39; mean age 24) with various degrees of left ventricular hypertrophy; all showed electrocardiographic ST and/or T wave abnormalities before scintigraphy. After dosing with dipyridamole-201 thallium, we found: a completely reversible perfusion defect in the apical and a partially reversible defect in the posterolateral wall of the left ventricle in 1 case; a partially reversible perfusion defect in the anterior and posterior walls of the left ventricle in 1 case; and a persistent anterolateral perfusion defect in 1 case. The remaining 10 patients showed no scintigraphic abnormalities. The fact that only 1 of our patients showed a completely reversible perfusion defect, possibly consistent with regional myocardial ischemia, suggests that ischemia does not play a major role in the pathogenesis of the cardiac involvement in Friedreich's ataxia.
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PMID:Myocardial perfusion in Friedreich's ataxia: assessment by dipyridamole thallium-201 imaging. 191 15

Two hundred fifty-eight patients were admitted to the hospital for suspected acute myocardial infarction. Electrocardiograms recorded on admission (initial ECG) and the most recent available electrocardiogram recorded before admission (previous ECG) were compared to determine whether changes from the previous to initial ECG predicted acute myocardial infarction or complications of coronary artery disease. Initial ECGs were classed as either positive or negative, with positive indicating either infarction, injury, ischemia, strain, left ventricular hypertrophy, left bundle branch block, or paced rhythm. Negative ECGs were those that did not include any of the positive criteria. Positive and negative ECGs were subgrouped as showing change or no change from previous ECG. We found that patients with a negative initial ECG that had changed from the previous ECG had a 2.1 times greater risk for requiring interventions than those patients whose ECGs were unchanged. We also found that patients with a positive initial ECG that had changed from the previous ECG had a greater risk for interventions (2.0 times), complications (2.6 times), life-threatening complications (4.2 times), and acute myocardial infarction (6.6 times) than the sum of patients in all other ECG categories. We conclude that change is a useful predictor for interventions in patients with negative initial ECGs and a useful predictor for interventions, complications, and acute myocardial infarction in patients with positive initial ECGs.
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PMID:Diagnostic and prognostic importance of comparing the initial to the previous electrocardiogram in patients admitted for suspected acute myocardial infarction. 174 89

Although exercise-induced ST segment depression is thought to be unreliable marker of myocardial ischemia in the presence of resting electrocardiographic changes, this conclusion is based on limited and disparate data from studies often lacking acceptable measures of ischemia. To determine the diagnostic accuracy of the ST segment response in a blinded prospective protocol, we compared ST deviation to thallium201 SPECT scintigraphy in 95 patients during exercise. Diagnostic accuracy was poor in the 95 patients with resting abnormalities: left bundle branch block (LBBB) = 70%, complete right bundle branch block (cRBBB) = 75%, incomplete right bundle branch block (incRBBB) = 79%, intraventricular conduction delay (IVCD) = 44%, left ventricular hypertrophy (LVH) = 59%, digitalis = 53%, compared with a diagnostic accuracy of 90% in 29 patients without resting changes. There were 20 false negative and 17 false positive ST segment responses. The extent and direction of resting ST deviation varied substantially and had no influence on diagnostic accuracy. The extent of change in ST deviation with exercise required for a positive response did not alter diagnostic accuracy: -1.0 mm = 61%, -1.5 mm = 63%, and -2.0 = 61%. While the location of regional ischemia did not influence the accuracy of ST segment analysis, a QRS duration less than 120 msec did improve diagnostic accuracy. Our data confirm that ST segment analysis with exercise testing is not reliable in patients with resting electrocardiographic abnormalities and demonstrates that accuracy is not improved by adjusting for either resting or exercise-induced ST segment changes or for location of the ischemic region.
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PMID:The effect of baseline electrocardiographic abnormalities on the diagnostic accuracy of exercise-induced ST segment changes. 213 78

The present study was undertaken to define the effects of left ventricular hypertrophy on postischemic recovery of myocardial performance and high energy phosphate metabolism. Hemodynamics and 31P-magnetic resonance spectra were monitored simultaneously in the isolated Langendorff-perfused rat heart during 30 minutes of ischemia and 30 minutes of reperfusion. Left ventricular hypertrophy was produced by either suprarenal aortic constriction or chronic thyroxine administration. In chronic pressure overload hypertrophy, minimal coronary resistance was significantly higher (p less than 0.001) and the loss of purine nucleosides in the coronary effluent during early reperfusion significantly larger (p less than 0.001) compared with both normal hearts and thyroxine-induced hypertrophied hearts. Postischemic recovery of the baseline values for left ventricular developed pressure and phosphorylation potential was 43 +/- 4% and 82 +/- 4%, respectively, in chronic pressure overload hypertrophied hearts; 86 +/- 4% and 91 +/- 3%, respectively, in normal hearts (chronic pressure overload hypertrophy versus normal hearts, p less than 0.001 and p less than 0.05); and 100 +/- 4% and 98 +/- 2%, respectively, in thyroxine-induced hypertrophied hearts (normal hearts versus thyroxine-induced hypertrophied hearts, p less than 0.05 and p less than 0.05). Recovery after reperfusion was not related to intracellular pH, ATP, phosphocreatine, or inorganic phosphate levels during ischemia. Also, recovery was not related to developed pressure or oxygen consumption before ischemia. However, recovery was inversely related to coronary resistance and directly related to coronary flow before ischemia. Thus, functional and/or anatomic alterations of the coronary vascular bed and a greater loss of purine nucleosides during reperfusion are likely responsible for the attenuated compensatory response to ischemia and reperfusion in left ventricular hypertrophy induced by chronic pressure overload. On the other hand, the excess muscle mass per se does not seem to alter recovery, since thyroxine-induced myocardial hypertrophied hearts responded at least as well as normal hearts.
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PMID:Postischemic recovery of mechanical performance and energy metabolism in the presence of left ventricular hypertrophy. A 31P-MRS study. 213 28


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