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

Evaluation of regional function and blood flow are used for describing regional myocardial performance. This approach however yields little if any information on regional substrate metabolism. The latter links function to blood flow. Persistence of metabolism, even though abnormal, may be critical for cell survival in myocardial ischemia. Fatty acid oxidation characteristically declines in ischemia while glycolytic flux may increase or be maintained. These changes can be evaluated with C-11 palmitate and F-18 2-fluoro 2-deoxyglucose (FDG) and leave characteristic "fingerprints" on cross-sectional positron emission tomography (PET) images. Blood flow and C-11 palmitate uptake are segmentally reduced while FDG uptake may be increased relative to flow or when compared to normal myocardium. The latter, a discordance between segmental blood flow and FDG uptake, signifies tissue viability and predicts recovery of segmental function after surgical revascularization. The pattern is more sensitive for detection of viable tissue than conventional techniques. It is also frequently seen in acute myocardial infarction. Segments with this pattern may regain function or not. Those segments that fail to improve function spontaneously may require aggressive treatment which could be decided based upon PET findings. Noninvasive detection of such "fingerprints" of myocardial ischemia by PET aids in establishing the presence of viable tissue and may therefore affect patient management. Development of quantitative criteria will be needed to more accurately predict possible tissue outcome which in turn will more clearly establish the need for more aggressive therapeutic measures in acute and chronic ischemic heart disease.
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PMID:Evaluation of "metabolic fingerprints" of myocardial ischemia. 348 8

The cardiovascular responses to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone were evaluated by upright bicycle ergometry during equilibrium-gated blood pool scintigraphy in 24 men, mean age 59 +/- 8 years, with chronic ischemic heart disease. Combined static-dynamic effort and the postprandial state elicited a peak cardiovascular response similar to that of dynamic effort alone; work load 643 +/- 156 and 638 +/- 161 vs 650 +/- 153 kg-m/min, respectively; heart rate 147 +/- 14 and 145 +/- 14 vs 143 +/- 17 beats/min; systolic pressure 195 +/- 26 and 200 +/- 25 vs 197 +/- 25 mm Hg; and rate-pressure product 286 +/- 48 and 292 +/- 55 vs 282 +/- 52. Heart rate, intraarterial systolic and diastolic pressures, rate-pressure product and ejection fraction were similar for the three test conditions at the onset of ischemia and at peak effort. The prevalence and extent of exercise-induced ischemic left ventricular dysfunction, ST-segment depression, angina pectoris and ventricular ectopic activity were also similar during the three test conditions. Direct and indirect measurements of systolic and diastolic blood pressure were highly correlated. The onset of ischemic ST-segment depression and angina pectoris correlated as strongly with heart rate alone as with the rate-pressure product during all three test conditions. The cardiovascular response to combined static-dynamic effort and to postprandial dynamic effort becomes more similar to that of dynamic effort alone as dynamic effort reaches a symptom limit. If significant ischemic and arrhythmic abnormalities are absent during symptom-limited dynamic exercise testing, they are unlikely to appear during combined static-dynamic or postprandial dynamic effort. This simplifies, the task of formulating guidelines for physical effort in patients with chronic ischemic heart disease, especially in providing "clearance" to perform avocational and vocational tasks involving combined static-dynamic and postprandial dynamic effort.
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PMID:Comparison of cardiovascular response to combined static-dynamic effort, postprandial dynamic effort and dynamic effort alone in patients with chronic ischemic heart disease. 628 Aug 92

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45

To compare acute effects of nitroglycerin (0.8 mg sublingually), nifedipine (5 ng/kg/min i.v.) and metoprolol (0.15 mg/kg i.v.) on normal, ischemic and scarred myocardial segments in man, we performed simultaneous hemodynamic and radionuclide measurements of left ventricular functions. Sixteen patients with isolated left anterior descending (LAD) disease were studied at rest and during exercise. Nine patients had angina and exercise-induced ischemia (LAD stenosis) and seven patients had previous transmural myocardial infarction and no ischemic changes during thallium imaging (LAD occlusion). The effects of the drugs on regional ejection fraction of the involved anteroseptal region and the normal posterolateral area were compared. Global ejection fraction at rest did not change after nitroglycerin, increased after nifedipine and decreased after metoprolol. In patients with ischemia, the exercise ejection fraction improved after all drugs due to increased regional ejection fraction in ischemic segments: i.e., a regional antiischemic effect evidenced by improved regional function could be demonstrated with all three agents. Regional ejection fraction increased from 35.8 +/- 19.5% to 66.2 +/- 15.2% (+/- SD) after nitroglycerin (p less than 0.001), to 61.7 +/- 8.7% after nifedipine (p less than 0.001), and to 48.4 +/- 7.0% after metoprolol (p less than 0.01). In regions of myocardial scar, regional ejection fraction was not changed after any drug. In normal areas, regional ejection fraction remained unchanged after nitroglycerin and nifedipine, but decreased after metoprolol. Despite similar antiischemic effects of all three drugs, underlying hemodynamic mechanisms were quite different and may provide a rationale for combined forms of treatment. These results may help to select optimal drug combinations to improve myocardial performance in patients with chronic ischemic heart disease.
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PMID:Comparative effects of nitroglycerin, nifedipine and metoprolol on regional left ventricular function in patients with one-vessel coronary disease. 640 Dec 30

In order to assess acute effects of nitroglycerin, nifedipine and metoprolol on normal, ischemic and scar myocardial segments in man, non-invasive hemodynamic and radionuclide measurements of left ventricular function were performed. Sixteen patients with single left anterior descending (LAD) disease were studied at rest and during exercise: 9 patients with angina and exercise-induced ischemia (LAD stenosis) and 7 patients with previous transmural myocardial infarction and no ischemic changes at thallium imaging (LAD occlusion). Effects on regional ejection fraction were compared between involved antero-septal and normal postero-lateral areas. Global ejection fraction at rest was unchanged after nitroglycerin, increased after nifedipine and decreased after metoprolol. In patients with ischemia, improvement in exercise ejection fraction after all drugs was due to increased regional ejection fraction in ischemic segments, i.e. a real anti-ischemic effect could be demonstrated. In regions of myocardial scar, regional ejections fraction was not changed after either drug. In normal areas, regional ejection fraction remained unchanged after nitroglycerin and nifedipine but decreased after acute beta-blockade. Despite the very similar anti-ischemic effects of all drugs, underlying hemodynamic mechanisms were quite different: Reduction in preload and afterload after nitroglycerin, vasodilatation and reflex sympathetic activity after nifedipine and reduction in double product and contractility after metoprolol. Thus, the mode of action of nitroglycerin, nifedipine and metoprolol on normal, ischemic and scar myocardial segments could be demonstrated in man. Non-invasive antianginal drug testing as shown in this study should allow optimal medical therapy for patients with chronic ischemic heart disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal drug effects on normal, ischemic and scar myocardial segments in man. 644 4

The effect of dobutamine on exercise performance was assessed in 20 patients with ischemic heart disease (CAD) and a positive stress test. These patients had a wide range of resting left ventricular ejection fraction (range 22% to 69%, mean 42%). Each patient entered a double-blind crossover study in which two identical exercise radionuclide ventriculograms were performed in patients on dobutamine, 5 micrograms/kg/min intravenously, or placebo. Dobutamine increased resting left ventricular ejection fraction. Although ejection fraction fell with dobutamine during submaximal exercise, it remained higher than with placebo. At peak exercise, ejection fraction fell to the same level on dobutamine as with placebo. Dobutamine diminished exercise time and time to ischemia while peak pressure-rate product was unchanged. Four of 20 patients developed complex ventricular premature beats, all while on dobutamine. Although useful when administered to resting patients with acute left ventricular failure, dobutamine's effects may be deleterious in exercising patients with chronic ischemic heart disease.
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PMID:The effect of dobutamine on exercise performance in patients with symptomatic ischemic heart disease. 669 Dec 44

The workup of a patient with chronic ischemic heart disease (IHD) before the selection of medical-surgical or medical therapy depends on multiple objective and subjective factors. These include symptoms, extent of anatomic disease (degree of coronary arteriosclerosis and left ventricular abnormalities), objective evidence of ischemia, extent of left ventricular dysfunction, and recent intercurrent ischemic events. In a minority of patients, a single factor is of overwhelming importance; e.g., the presence of severe left main coronary artery narrowing in a symptomatic patient indicates surgery is a better choice, whereas evidence of advanced left ventricular dysfunction suggests that surgery is likely to be risky and of limited help to the patient. In most instances, multiple factors should be considered before making a recommendation. The patient should be placed in the appropriate clinical subset and the objective factors that are most important in determining survival should be evaluated. Hence, an exercise electrocardiographic study to evaluate symptoms and exercise tolerance in a patient with angina pectoris and radioventriculographic studies with exercise to estimate left ventricular performance in a patient who complains of fatigue and breathlessness are superior to the subjective interpretations of routine clinical examinations. Asymptomatic patients and those with excellent exercise tolerance pose the most difficult decisions. Perhaps serial (even annual) noninvasive evaluation is appropriate in such patients in light of the current uncertainty about how to manage them. Laboratory tests should be used selectively, systematically and sequentially. The high cost of many of the examinations is reason to avoid duplication. When noninvasive evaluation can answer the question being posed and the cost of hospitalization avoided, this should be done. However, there is little reason to perform noninvasive examinations that do not answer the clinical question being asked; hence, in many patients it is appropriate to proceed directly to coronary arteriography rather than to perform a variety of "screening" examinations before this procedure.
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PMID:The reasonable workup before recommending medical or surgical therapy: an overall strategy. 697 29

The ultrastructure of the contractile myocardium of the left ventricle of the heart in chronic ischemic heart disease was studied in 24 puncture myocardial biopsies. Marked dystrophic changes were revealed in the cell organelles, both in the membrane systems and in the myofibrillary apparatus, which the authors believe were caused by long-term increasing ischemia of the organ. Besides dystrophy, signs of intracellular regeneration were found in some myocytes. These signs were the presence of euchromatin in the nuclei of the myocytes, and increase in the amount of RNA granules and granular sarcoplasmic reticulum in the sarcoplasm. The prevalence of dystrophic changes on the level of the myocyte ultrastructure may be among the causes of cardiac insufficiency in patients with chronic ischemic heart disease.
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PMID:[Ultrastructure of the contractile myocardium in chronic ischemic heart disease]. 739 78

Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.
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PMID:[An evaluation of the plastic function of the cardiomyocytes by silver staining of the nucleoli in patients operated on for ischemic heart disease]. 752 67

The objective of this study was to determine whether basic fibroblast growth factor (bFGF), a known angiogenic factor, can promote new vessel growth when infused within the pericardial space in a model of chronic myocardial ischemia. Intravenous angiotensin II (AII) was infused to induce left ventricular hypertrophy and concomitant ischemia in New Zealand white rabbits. Basic FGF was infused into the intrapericardial space with an osmotic pump. Animals were assigned to one of four groups: group 1 received intrapericardial bFGF and intravenous AII, group 2 received intrapericardial bFGF and intravenous saline solution, group 3 received intrapericardial albumin and intravenous AII, and group 4 received intravenous AII only. Epicardial angiogenesis was graded histologically on a scale of 0 to 2. Animals receiving intravenous administration of AII displayed left ventricular hypertrophy that disproportionately affected the interventricular septum with a wall thickness of 5.62 +/- 1.00 mm versus 3.98 +/- 0.61 mm in the AII group and the saline solution control group, respectively (p < 0.005). A highly localized angiogenic effect of bFGF was observed. The mean angiogenesis scores were 1.9, 1.4, 1.3, and 0.2 (p < 0.001) with an angiogenesis score of 2 (marked increase in vascularity) noted in 86%, 40%, 43%, and 0% of hearts in groups 1 through 4, respectively. We conclude that intrapericardial bFGF enhances new epicardial small-vessel growth in a rabbit model; furthermore this effect is enhanced in the presence of left ventricular hypertrophy.
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PMID:Intrapericardial basic fibroblast growth factor induces myocardial angiogenesis in a rabbit model of chronic ischemia. 753 43


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