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

Silent myocardial ischemia was studied in 100 patients with coronary heart disease (CHD), proved by the coronary arteriogram (at least one major coronary artery narrowed by > or = 50%). The study demonstrated that 51 of 100 patients with CHD had episodes of myocardial ischemia by Holter monitoring. In the 51 patients, during daily activities, through 24-hour Holter monitoring, 239 transient episodes of ST depression were detected, 161 of the total were asymptomatic (67.4%). There were no statistically significant differences in the heart rate and the product of heart rate and systolic blood pressure before ST depression between asymptomatic and symptomatic episodes. The heart rate at the time of maximal ST depression during both asymptomatic and symptomatic ischemia increased by 13 and 22 beats/min, respectively, over those before ST depression (P < 0.01); whereas the increase in heart rate during symptomatic ischemia was more significant than during asymptomatic ischemia (P < 0.01). The increase of product of heart rate and systolic blood pressure at the time of maximal ST depression during asymptomatic and symptomatic ischemia were 22.2 and 35.4, respectively, over those before ST depression (P < 0.01). The incidence of silent ischemic episodes in patients with single vessel disease was 81.7% and those with multivessel disease was 61.3% (P < 0.01). The frequency of silent ischemic episodes was maximal (36% of total number of ischemic episodes) between 6 a.m. and 12 a.m. during 24-hour, whereas the incidence of silent ischemic episodes in patients with single vessel disease was similar to that in patients with multivessel disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary heart disease and silent myocardial ischemia]. 147 87

A 68-year-old man with known coronary heart disease experienced rapidly progressive cardiac dysfunction and was found to have occult cardiac amyloidosis at autopsy. The amyloidosis was undiagnosed during life and initially at autopsy. Marked diffuse involvement of the intramural coronary arteries by amyloid deposits resulted in severe luminal compromise of numerous medium and small vessels. The myocardium proper was virtually spared from amyloid deposits. Amyloid-related coronary narrowing contributed to cardiac ischemia and sudden death. The significance of amyloid coronary disease in this patient relates primarily to the difficulty in considering the diagnosis when other reasons for cardiac signs and symptoms preexist. Also, the adverse effects of amyloid coronary disease may be profound without direct myocardial involvement.
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PMID:The clinical problem of occult cardiac amyloidosis. Forensic implications. 147 28

Objective signs of myocardial ischemia without angina pectoris or its equivalents define the syndrome of silent myocardial ischemia. Its significance lies in the prevalence and prognostic implications. As a prevalence, asymptomatic coronary heart disease can be found in 2.5% of men 40 to 60 years old. Silent myocardial ischemia is frequently found in patients with unstable coronary syndromes. The Framingham Study showed 25% of all myocardial infarctions as unrecognized by patients and physicians. The prognostic implications of silent myocardial ischemia are shown in large studies on prognosis of pathologic exercise-ECG's. Asymptomatic patients with pathologic exercise-ECG have always been recognized as having a significantly increased risk of myocardial infarction and death. Recently, many studies showed a worse prognosis for patients with asymptomatic transient ischemia on Holter-ECG. This can be found in patients with stable angina pectoris, unstable angina pectoris, patients with peripheral arterial disease, and patients after myocardial infarction. It becomes clear that prognosis is not defined by the pain, but by the severity of ischemia. Silent ischemia has to be viewed together with the severity of the underlying coronary heart disease. This synopsis will define the necessary steps for further diagnosis and treatment.
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PMID:[Clinical importance of silent ischemia]. 160 22

Since January 1983 one surgeon of our team has performed 200 infrainguinal arterial reconstructions. Our patients had a mean age of 72 years and suffered from multiple concomitant diseases (coronary heart disease 35%, cerebro-vascular insufficiency 15%, hypertension 49% and diabetes mellitus 34%). The indication for arterial reconstruction was a chronic critical ischemia in every case. 154 autologous veins and 46 PTFE prosthesis had to be implanted. The former consisted in 64% in a femoropopliteal and in 35% femorodistal bypass graft; respective values of the latter group were 80% and 20%. The cumulative survival rates of two collectives were nearly identical. More than 50% of our patients died in the 4 years observation period. The life table patency rates differed statistically significant (p less than 0.001). The cumulative 5 year patency amounted to 85% in case of a vein graft and to 43% if a PTFE prosthesis was inserted. Extremely poor results were achieved in case of a PTFE prosthesis with a distal anastomosis to a single crural artery; just one out of 6 procedures was successful after two years.
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PMID:[Five years experience with infra-inguinal arterial reconstruction: a comparison of venous with PTFE bypass]. 162 37

Successful transluminal coronary angioplasty (PTCA) should improve left ventricular systolic function. To assess the effect of this procedure 25 patients with coronary heart disease were examined before and 3-to 5 days after successful PTCA with electrocardiographic treadmill exercise test, and exercise two-dimensional echocardiography (modified Bruce protocol). Echocardiographic examination was obtained prior to and immediately following exercise. Left ventricular ejection fraction and segmental wall motion at the baseline and immediately after exercise were assessed. Electrocardiographic evidence of ischemia was found in 16 of 25 patients prior to PTCA and in 9 patients after PTCA. Following angioplasty, exercise duration was increased and the exercise-induced angina rate was significantly decreased. Ejection fraction did not change significantly in patients prior and after PTCA (52 +/- 10% versus 55 +/- 16%, p = NS). Following angioplasty, ejection fraction increased from 55 +/- 10% (rest) to 64 +/- 11% (exercise) (p less than 0.001). New exercise-induced echocardiographic segmental wall motion abnormalities were found in 16 of 25 patients prior to PTCA and in only one patient following PTCA. Significant improvement of ejection fraction and segmental wall motion were also observed in 11 patients with old myocardial infarction subjected to successful angioplasty of infarct-related coronary artery. Opposite to post-exercise results, the resting mean values of these echocardiographic parameters did not differ significantly between pre and post-PTCA examinations. These data demonstrate an improvement in systolic left ventricular function and better exercise tolerance following successful PTCA. This occurs also in patients with old myocardial infarction after angioplasty of infarct-related coronary artery. Two-dimensional exercise echocardiography may be helpful in assessing the early results of successful angioplasty.
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PMID:[PTCA and left ventricular systolic function (evaluation by exercise two-dimensional echocardiography)]. 162 8

The Cardiovascular Health Study (CHS) is a population-based, longitudinal study of coronary heart disease and stroke in adults aged 65 years and older. The main objective of the study is to identify factors related to the onset and course of coronary heart disease and stroke. CHS is designed to determine the importance of conventional cardiovascular disease (CVD) risk factors in older adults, and to identify new risk factors in this age group, especially those that may be protective and modifiable. The study design called for enrollment of 1250 men and women in each of four communities: Forsyth County, North Carolina; Sacramento County, California; Washington County, Maryland; and Pittsburgh, Pennsylvania. Eligible participants were sampled from Medicare eligibility lists in each area. Extensive physical and laboratory evaluations were performed at baseline to identify the presence and severity of CVD risk factors such as hypertension, hypercholesterolemia and glucose intolerance; subclinical disease such as carotid artery atherosclerosis, left ventricular enlargement, and transient ischemia; and clinically overt CVD. These examinations in CHS permit evaluation of CVD risk factors in older adults, particularly in groups previously under-represented in epidemiologic studies, such as women and the very old. The first of two examination cycles began in June 1989. A second comprehensive examination will be repeated three years later. Periodic interim contacts are scheduled to ascertain and verify the incidence of CVD events, the frequency of recurrent events, and the sequellae of CVD.
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PMID:The Cardiovascular Health Study: design and rationale. 166 7

Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminished flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with beta-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.
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PMID:New concepts in ischemia prevention. 172 49

A sample of 45 patients with a history of coronary heart disease and documented myocardial ischemia during exercise testing were evaluated in an investigation of the possible relationships between psychological factors (depression and Type A behavior pattern), plasma beta-endorphin response and pain experience during maximal exercise-induced ischemia. Depression was assessed using the MMPI-D subscale, while Type A was evaluated using the Structured Interview. All patients developed ischemia during exercise as defined by ST-segment depression; however, only 18 patients reported anginal pain. Patients with high depression scores (MMPI-D greater than or equal to 70; n = 13) showed lesser increases in plasma beta-endorphin levels, tended more often to report anginal pain and rated pain as more severe during exercise than patients with low depression scores (MMPI-D less than 60; n = 18). Hemodynamic responses and severity of ischemia (assessed by ejection fraction changes and wall-motion abnormalities) did not differ between depression groups. Even after adjustment for group differences in exercise duration, depression was significantly associated with a lesser beta-endorphin response in the sample as a whole and, among patients reporting angina, with earlier pain onset and greater pain duration and severity. In contrast, when Type A versus B/X subgroups were compared, no differences in pain experience, beta-endorphin response or measures of ischemia were obtained. These findings suggest that in patients with ischemic heart disease, there may be a relationship between depression and anginal pain which may in part involve a blunted or absent beta-endorphin response.
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PMID:Depression and type A behavior pattern in patients with coronary artery disease: relationships to painful versus silent myocardial ischemia and beta-endorphin responses during exercise. 175 50

The blood levels of 6-keto-PGE1 alpha and thromboxane B2 were measured in the coronary sinus of 15 males during and just after a spontaneous myocardial ischemic episode. The comparison was made in 30 males with coronary heart disease in the presence of exercise-induced angina in whom coronary sinus blood samples were taken during myocardial ischemia provoked by pacing and 6 males suffering from cardialgias without signs of coronary atherosclerosis. The patients with spontaneous anginal attacks had lower baseline 6-keto-PGE1 alpha (179.0 +/- 47.8 pkg/ml) than those with exercise-induced angina (336.0 +/- 65.7 pkg/ml; p less than 0.1). This difference became greater during ischemia (165.0 +/- 49.0 and 350.0 +/- 69.5 pkg/ml, respectively, p less than 0.05) and just after its elimination (166.0 +/- 48.7 and 413.0 +/- 76.0 pkg/ml, respectively, p less than 0.05). Coronary sinus blood thromboxane B2 levels were not substantially different in the presence or absence of myocardial ischemia. Thus, a decrease in the prostacyclin-forming function of the coronary endothelium plays a definite role in the genesis of spontaneous myocardial ischemic episodes.
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PMID:[Coronary sinus blood thromboxane and prostacyclin in spontaneous myocardial ischemia]. 179 81

Increased sympathetic activity is assumed to contribute substantially to the occurrence of malignant arrhythmias in patients with coronary heart disease, since the rate of sudden cardiac death is significantly reduced by beta-adrenoceptor blockade, but not by antiarrhythmic agents such as flecainide or encainide. During acute myocardial ischaemia, adrenergic stimulation of the ischaemic myocardium is independent of plasma catecholamines. Rather, it is caused by the combination of excessively high local noradrenaline concentrations and an enhanced responsiveness of the myocyte to catecholamines. Myocardial ischaemia of 15 min duration results in a 100-fold increase in catecholamine concentrations within the extracellular space of the ischaemic zone, a two-fold increase in functionally coupled alpha-adrenoceptors, and a 30% increase in beta-adrenoceptors. Within the first 10 min of ischaemia, the myocardium is protected from excessive catecholamine release. Ischaemia-associated metabolic alterations, such as extracellular potassium accumulation, acidosis, and especially the accumulation of adenosine reduce the transmitter release caused by central sympathetic activation. Furthermore, the functional neuronal amine reuptake (uptake1) prevents excessive local accumulation of noradrenaline. With progression of ischaemia to more than 10 min, local nonexocytotic catecholamine release becomes predominant. This release is independent of central sympathetic nerve activity, availability of extracellular calcium, activation of both neuronal calcium channels and protein kinase C, and it is not accompanied by the release of sympathetic cotransmitters such as neuropeptide Y. It has been demonstrated to be nonexocytotic and to be caused by a carrier-mediated transport of noradrenaline from the sympathetic nerve ending into the synaptic cleft. This release is not modulated through presynaptic receptors. It is, however, suppressed by blockers of uptake1 and by inhibitors of sodium-proton exchange. Depletion of cardiac catecholamine stores by chronic surgical or chemical sympathectomy effectively suppresses malignant arrhythmias induced by experimental coronary ligature. Accordingly, inhibitors of nonexocytotic noradrenaline release, such as uptake1 blocking agents or sodium-proton exchange inhibitors, effectively reduce the occurrence of ischaemia-associated ventricular fibrillation, emphasizing the relevance of nonexocytotic release mechanisms in myocardial ischaemia.
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PMID:Catecholamine release and arrhythmias in acute myocardial ischaemia. 180 38


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