Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, atrophy, degenerations of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7. amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.
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PMID:An epidemiologic and histopathological study of sudden cardiac death in Osaka Medical Examiner's Office. 263 29

The Minnesota Heart Survey assessed attack rates of MI in Twin Cities residents ages 30-74 years in 1970 and 1980. The age-adjusted attack rate per 100,000 of definite MI was similar in 1970 (174.2) and 1980 (179.9) p greater than 0.05, using ECG, chest pain, and blood enzyme concentrations of aspartate transaminase and/or lactic dehydrogenase as criteria. The attack rate of definite MI also remained constant when autopsy findings were included in the algorithm, 197.0 in 1970 and 191.4 in 1980 (p greater than 0.05). Adding creatine phosphokinase (CPK) and CPK-MB isoenzyme to the algorithm increased the rate of definite MIs from 209.0 in 1970 to 277.0 in 1980 (p less than 0.001). Interpretation of long-term trends in coronary heart disease morbidity is highly dependent upon variables used to validate cases. Care must be taken to maintain consistent criteria to avoid bias due to improvements in diagnostic techniques over time which increase sensitivity for detection of cardiac ischemia.
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PMID:The effects of diagnostic criteria on trends in coronary heart disease morbidity: the Minnesota Heart Survey. 264 74

More recent long-term ECG studies in patients with coronary heart disease have resulted in a focusing of interest on silent myocardial ischemia. Diagnostically, ECG changes suspicious for ischemia should always be confirmed by a second criterion. It has been found that differences between silent myocardial ischemia and angina pectoris are to be found mainly in the origination, conduction and perception of pain, and not in the underlying ischemia. Accordingly, prognostic studies have also shown that, in common with the presence of angina pectoris, the demonstration of silent myocardial ischemia is also a prognostically unfavorable sign. In severe ischemia, the indication for therapy is based on the prognosis of the patient; however, there have so far been no studies aimed at showing whether the prognosis of the patient can be improved over the long term by drug treatment.
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PMID:[Value of silent myocardial ischemia]. 264 90

As an introduction the main aspects concerning clinical picture, subgroups, pathophysiology, frequency, prevalence and incidence, diagnosis, prognosis and therapy of silent ischemia are summarized: 1) CLINICAL PICTURE: Transient silent ischemia (SMI), silent infarction, relationship to sudden cardiac death, ischemic "cardiomyopathy". 2) Subgroups of SMI: SMI patients (always symptomatic patients without myocardial infarction, after infarction, after stable or unstable angina pectoris, after coronary angioplasty, and after bypass surgery). SMI episodes in otherwise symptomatic patients with coronary heart disease (without myocardial infarction, after infarction, with stable or unstable angina, after coronary angioplasty and after bypass surgery). 3) PATHOPHYSIOLOGY: SMI patients: generally reduced sensitivity to pain. SMI episodes: differences in severity and duration of ischemia. 4) Frequency: Approximately one-third of all provoked ischemic episodes are silent (independent of the mode of provocation and the ischemia indicators used), two-thirds of all spontaneous ischemic episodes are silent. 5) Prevalence and incidence: 2-5% of all healthy males aged 40-59, and 20-30% of all postinfarction patients are SMI-patients; 60-90% of all symptomatic patients with coronary heart disease have additional SMI-episodes. 6) DIAGNOSIS: screening by means of exercise ECG in patients at high risk for coronary heart disease, and in patients working in specific professions (like busdrivers, pilots, etc.). Systematic screening in postinfarction patients, in patients after unstable angina, after coronary angioplasty or bypass surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Silent myocardial ischemia]. 268 55

At a dosage of 75 mg b.i.d., gallopamil retard represents a suitable medication for the treatment of both symptomatic and asymptomatic ischemic episodes, as could be demonstrated in patients with coronary heart disease ascertained by angiography, positive exercise testing, and more than five ischemic episodes in Holter monitoring over 48 h. The results of our study furnish proof that more than 60% of ischemic episodes recorded in patients with stable angina pectoris during Holter monitoring over 48 h, have been asymptomatic, i.e., silent. It must thus be postulated that effective antianginal therapy must be able to suppress both symptomatic and asymptomatic ischemic episodes. This should be documented by Holter monitoring over 48 h. It has not been established yet which criteria: duration of ST-segment depression, frequency of ischemic episodes, or area integral of ST-segment depression, furnish the most adequate parameters for assessment of ischemia. Assessment of the three criteria, taken together, is likely to be most reliable and should thus, in particular, be adhered to in evidencing efficacy in an antianginal drug trial.
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PMID:[Effectiveness of retard gallopamil in patients with stress-induced ST-segment depression and silent myocardial ischemias]. 269 71

Coronary disease causes the majority of perioperative complications after peripheral vascular surgery. Twenty-four patients with stable coronary disease undergoing peripheral revascularization were studied using continuous electrocardiographic monitoring to determine the incidence of perioperative asymptomatic myocardial ischemia and its relation to postoperative clinical ischemic events. Patients were monitored preoperatively (17 +/- 1 hours), intraoperatively and postoperatively (29 +/- 2 hours) using 4-channel calibrated amplitude-modulated units. Fifteen patients (63%) had early postoperative silent ischemia; 3 also had preoperative silent ischemia and 5 intraoperative transient ischemia. Patients with and without silent ischemia had similar clinical characteristics, perioperative antianginal medications and postoperative episodes of hemodynamic instability. However, 8 of 15 patients (53%) with silent ischemia had postoperative clinical ischemic events (2 had myocardial infarction, 2 had new congestive heart failure and 4 had new rest angina), versus only 1 of 9 patients (11%) without silent ischemia who had angina (p less than 0.05). Early postoperative silent myocardial ischemia occurs frequently after vascular surgery and is associated with postoperative clinical ischemic events.
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PMID:Frequency and significance of early postoperative silent myocardial ischemia in patients having peripheral vascular surgery. 281 64

The concept of the total ischemic burden includes all types of ischemia encompassing both silent and symptomatic ischemic episodes. This concept is currently causing a re-evaluation of current therapeutic goals for patients with coronary heart disease. Although the mechanism of cardiac pain is still unclear, we do have some information about other pathophysiologic mechanisms at work in this disorder. We think of ischemia as occurring secondary to reduced supply (primary ischemia), increased demand (secondary ischemia), or a combination of the two (mixed ischemia). Because of the lower heart rate associated with many episodes of ischemia during everyday activities, suggesting that vasoconstriction is playing a role in the patient's supply/demand imbalance, calcium antagonists appear to be particularly useful agents for the treatment of vasoconstriction in patients with angina.
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PMID:Total ischemic burden: definition, mechanisms, and therapeutic implications. 287 33

Factors contributing to the development of exercise-induced painful ischemia, such as actions of the central nervous system and catecholamines, have been well identified, but the mechanisms by which nonexercise-related silent episodes of ischemia are provoked are unknown. Possible mechanisms receiving much study in recent years are those having the potential to influence the myocardial oxygen supply-demand relation. Beta-adrenergic receptor stimulations, by increasing myocardial oxygen demand through augmentation of heart rate and contractility (beta 1), may mediate responses that cause ischemia or perpetuate ischemic episodes induced by other means. Other receptors (beta 2) may mediate coronary and peripheral vascular constriction, limiting myocardial oxygen supply and further increasing myocardial oxygen demand. Studies have investigated the effect of beta blockade on ischemic episodes in patients with a variety of clinical forms of coronary heart disease. Beta blockade has been shown to reduce the frequency and duration of silent and painful ischemic episodes in patients with effort angina and rest angina. The data suggest that heart rate and perhaps other changes observed with use of beta blockade play an important role in silent ischemia; heart rate at specific times throughout the day, particularly in the late A.M., and the increase in heart rate seen in conjunction with silent ischemic episodes are all decreased with administration of beta blockade. Results of a recent study focusing only on silent ischemia showed that beta-blocker treatment with metoprolol, compared with placebo, significantly reduced total silent ischemic time (frequency and duration of episodes) in all periods examined.
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PMID:Beta-adrenergic blockers in silent myocardial ischemia. 289 28

A 68 years old female patient was admitted with thoracic pain and fever (40.0 degrees C). A coronary heart disease was known. The liver was enlarged, the cholestatic enzymes elevated without bilirubinaemia. In the blood culture gram-negative bacilli was found. Our diagnosis: septic cholangitis, coronary ischemia. She was better by antibiotic therapy, the fever fell. Few days later she suddenly died. Autopsy demonstrated a serious arteriosclerosis of the aorta, an aneurysm on the aortic arc with chronic bleeding in the environmental tissue with inflammation and coronary arteriosclerosis. The liver was normal.
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PMID:[Thoracic dissecting aortic aneurysm. Contribution to the differential diagnosis of increased enzymes indicating cholestasis, fever and thoracic pain]. 289 6

Cigarette smoking has been causally linked to coronary heart disease. To investigate the effect of smoking on the activity of ischemic heart disease, 65 patients with chronic stable manifestations of coronary disease and a positive exercise tolerance test underwent continuous ambulatory monitoring to quantify the amount of ischemic ST segment depression during daily life. Twenty-four smokers were compared with 41 nonsmokers for frequency and duration of electrocardiographic signs of ischemia during 24 hours. A total of 4,968 hours of ambulatory monitoring were analyzed. The frequency of episodes was three times as often (median) and the duration of ischemia was 12 times longer (median duration, 24 vs 2 min/24 h) in smokers than nonsmokers. This finding remained statistically significant when a number of potentially confounding factors were controlled by means of logistic regression. This study shows that patients with coronary artery disease who smoke have significantly and substantially more active myocardial ischemia during daily life than patients who do not.
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PMID:Effect of smoking on the activity of ischemic heart disease. 290 79


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