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

The ability of maximal exercise thallium testing to stratify patients after non Q wave myocardial infarction was prospectively examined in 20 patients. Patients were enrolled in the study if there was no evidence of residual ischemia nor congestive heart failure during initial hospitalization. The thallium exercise test showed four patients to be at high risk, three of whom had successful revascularization. The remaining 16 patients were considered to be at low risk. There were no re-admissions for unstable angina, no myocardial infarctions and no deaths in the follow-up period (average 15 months). Thus patients with no evidence of early ischemia, no signs of left ventricular failure and a negative maximum thallium exercise test are at low risk following non Q wave myocardial infarction.
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PMID:Risk stratification in patients with non Q wave myocardial infarction: a role for thallium exercise testing. 227 99

Abdominal aortic aneurysmectomy (AAA) results in thromboxane (Tx)A2 generation, a rise in mean pulmonary artery pressure (MPAP), leukopenia, and noncardiogenic pulmonary edema. This study tests whether mannitol, a hydroxyl radical scavenger, modifies these events. Patients received mannitol 0.2 g/kg (n = 14) or saline (n = 12) intravenously before infrarenal aortic clamping. With saline, 30 minutes after clamping, plasma TxB2 levels rose from 124 to 290 pg/mL (p less than 0.01), and MPAP rose from 19 to 27 mmHg (p less than 0.01). Aortic clamp release led to further increases in plasma TxB2 to 378 pg/mL (p less than 0.01) and MPAP to 34 mmHg (p less than 0.01). The white blood count (WBC) fell from 9800 to 4400/mm3 (p less than 0.01). Four to eight hours after surgery, physiologic shunting (Q[sc]S[xsc]/Q[sc]T[xsc]) rose from 9% to 20% (p less than 0.01) and peak inspiratory pressure (PIP) increased from 22 to 32 cmH2O (p less than 0.01). Chest radiography demonstrated pulmonary edema while the pulmonary wedge pressure was 12 mmHg, excluding left ventricular failure. By 24 hours pulmonary edema resolved and the PIP and PaO2 returned to baseline. Mannitol treatment relative to saline, during and after aortic clamping reduced plasma TxB2 levels to 155 and 198 pg/mL, respectively (p less than 0.01); MPAP to 21 and 26 mmHg (p less than 0.01); minimized the decline in WBC to 5850/mm3 (p less than 0.01), and the postoperative rise in Q[sc]S[xsc]/Q[sc]T[xsc] to 12%, and PIP to 28 cmH2O (both p less than 0.01). Chest radiography showed no pulmonary edema. Finally in vitro studies documented that mannitol 1 to 10(-4)M, but not dextrose, in a dose-dependent manner inhibited Tx synthesis by ADP-activated platelets. These data indicate that mannitol maintains pulmonary function after AAA by limiting ischemia-induced thromboxane synthesis.
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PMID:Pulmonary edema after aneurysm surgery is modified by mannitol. 1257 26

This study investigates the possible role of oscillatory release of calcium from sarcoplasmic reticulum in the genesis of ventricular arrhythmias during acute myocardial ischemia and reperfusion in isolated rat hearts. We used ryanodine and caffeine, which are known to modulate the oscillatory release of calcium from sarcoplasmic reticulum. During 30 minutes of left main coronary artery ligation, all 13 control hearts developed ventricular premature beats (number of beats, 225 +/- 51) and ventricular tachycardia (duration, 123 +/- 21 seconds); five hearts developed ventricular fibrillation. In a separate series of experiments, reperfusion after 15 minutes of coronary artery ligation caused ventricular fibrillation to occur within 15 seconds in all 12 hearts. Ryanodine (10(-9) to 10(-7) M) abolished ventricular arrhythmias during coronary artery ligation and prevented reperfusion ventricular fibrillation. Ryanodine (10(-9), 10(-8), and 10(-7) M) caused 15%, 23%, and 74% decreases in the maximal rate of rise of left ventricular pressure development and 20%, 32%, and 85% decreases in the maximal rate of fall of left ventricular pressure development, respectively, prior to coronary artery ligation. During acute myocardial ischemia, ryanodine 10(-9) M maintained and 10(-8) M impaired left ventricular function; 10(-7) M caused left ventricular failure. Coronary perfusion rate did not increase during ischemia. Antiarrhythmic activity occurred independent of preservation of high energy phosphates, reduction in tissue lactate, or tissue cyclic adenosine monophosphate in the ischemic myocardium. Caffeine 10(2) M decreased the incidence of ventricular arrhythmias during ischemia and upon reperfusion; protection occurred coincident with development of diastolic contracture. Caffeine increased ischemic tissue cyclic adenosine monophosphate content and worsened tissue energy status.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart. 282 12

It is important to select patients in the convalescent phase of acute myocardial infarction in whom knowledge of coronary anatomy may identify those potentially suitable for intervention aimed at improving prognosis. However, differing guidelines have been proposed, and by applying some of these guidelines to our large database of patients after acute myocardial infarction, several problem areas were identified. These include lack of considering patients with resting ischemia beyond day 5 of hospitalization, management of patients with reduced ventricular function or patients not exercise tested, and the role of coronary angiography in the elderly. Based on this experience and further analysis in 1,848 patients surviving beyond day 5 of hospitalization, a modified decision scheme for coronary angiography was developed and then tested in a second population (n = 780). In the new scheme, patients over 75 years of age are considered individually. Those under 75 years of age with severe resting ischemia in the hospital at any time beyond the first 24 hours (18% mortality between day 6 and year 1), and hospital survivors with a history of previous myocardial infarction and clinical or radiographic signs of left ventricular failure in the hospital (25% 1-year mortality after discharge), are recommended for coronary angiography. Among the remaining patients, some will perform an exercise test, and those with an ischemic response or poor workload (11% 1-year mortality) are also assigned to coronary angiography. When an exercise test is not performed, a resting radionuclide left ventricular ejection fraction is recommended, and coronary angiography is considered if the value lies between 0.20 and 0.44 (12% 1-year mortality). This relatively simple scheme does not make general recommendations in the elderly, considers patients with in-hospital left ventricular failure or reduced left ventricular function or both, and approaches the problem of patients who do not perform an exercise test. This general approach would avoid early coronary angiography in patients with an average 1-year mortality risk after discharge of 3% and recommend coronary angiography in those at increased risk (average mortality rate, 16%) who make up about 55% of this population under 75 years of age.
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PMID:A decision scheme for coronary angiography after acute myocardial infarction. 291 48

Limb ischemia in experimental animals leads to white blood cell (WBC) and thromboxane (Tx)A2 dependent pulmonary dysfunction. This study examines the pulmonary sequelae of lower torso ischemia in 20 consecutive patients aged 63 +/- 5 years (mean +/- SEM) who underwent elective abdominal aortic aneurysm surgery. After 30 minutes of aortic cross-clamping, plasma TxB2 levels had risen from 77 +/- 26 pg/ml to 359 +/- 165 pg/ml (p less than 0.01) and was temporally related to increases in mean pulmonary artery pressure (MPAP) from 18 +/- 1 to 23 +/- 3 mmHg (p less than 0.01), as well as to increases in pulmonary vascular resistance (PVR) from 0.07 +/- 0.02 to 0.12 +/- 0.02 mmHg sec/ml (p less than 0.01). Each time that the aortic clamp was repositioned and with final declamping, after 83 +/- 10 minutes, there were further increases in MPAP to a peak of 32 +/- 2 mmHg (p less than 0.01) and in PVR to 0.26 +/- 0.030 mmHg sec/ml (p less than 0.01), corresponding to a plasma TxB2 level of 406 +/- 177 pg/ml (p less than 0.01). MPAP and PVR returned to baseline values within 30 minutes of declamping. Ten minutes after removal of the aortic clamp, platelet levels had fallen from 180 +/- 41 to 97 +/- 17 X 10(3)/mm3 (p less than 0.01) and WBC levels from 8900 +/- 1100 to 4700 +/- 400/mm3 (p less than 0.01). Both platelets and WBC returned towards normal levels, but at 24 hours, while WBC was elevated at 13000 +/- 900/mm3 (p less than 0.01), platelets were 44% of baseline at 135 +/- 14 X 10(3)/mm3 (p less than 0.01). Four to 8 hours after surgery, pulmonary dysfunction was manifest by increases in physiologic shunt from 9 +/- 2% to 16 +/- 2% (p less than 0.01), and peak inspiratory pressure (PIP) from 23 +/- 2 to 33 +/- 2 cmH2O (p less than 0.01). Chest radiography demonstrated interstitial pulmonary edema in all patients, whereas pulmonary artery wedge pressure was 12 +/- 2 mmHg, excluding the possibility of left ventricular failure. After 24 hours, pulmonary edema had resolved, and the PIP and PaO2 had both returned to baseline. These data indicate that reperfusion of the ischemic lower torso leads to the synthesis of TxA2, an event temporally related to pulmonary hypertension and transient leukopenia with subsequent pulmonary microvascular injury manifest by interstitial edema.
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PMID:Noncardiogenic pulmonary edema after abdominal aortic aneurysm surgery. 291 66

The radiologic appearance of atypical cardiogenic pulmonary edema (ACPE) is presented in 10 cases admitted from 1983 to 1985, with age ranges from 74 to 89, and with diagnosis of ischemic heart disease, with myocardial infarction in 50% of them. Clinically they had asthenia, adynamia and anorexia in 80%, cough and weight loss in 50%. All of them had tachycardia, pulmonary rales and 50% pericardial rub. ECG showed in 80% anterior subepicardial ischemia, 60% posteroinferior subepicardial ischemia, 60% bifascicular block, and 50% left anterior fascicular block. Chest films were interpreted at first as pulmonary fibrosis in 90% of the cases with superior lobe involvement in 50%. Heart enlargement was present in 50%. A chronic lung disease was disclosed on clinical and pulmonary physiological grounds. It is concluded that asthenia, adynamia and anorexia were atypical manifestations of heart failure in the elderly. Silent myocardial infarction was observed in half of our patients and it was complicated with pericardial involvement in 50%. Irregular distribution of fluids in pulmonary edema was attributed to anatomic changes in elder lung. These atypical behaviour of pulmonary edema, has been misinterpreted on radiologic basis with pulmonary infection, tumours, metastasis or fibrosis. Those radiologic changes disappeared or improved in 72 hrs. with treatment of left ventricular failure.
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PMID:[Radiologic characteristics of cardiogenic pulmonary edema in the elderly]. 296 66

Cardiac failure remains a life-threatening complication for certain patients undergoing intracardiac repair. Despite improvements in surgical techniques, methods of myocardial protection, and postoperative care, patients are frequently at risk to develop postoperative low output syndrome. Approximately 1% of cardiac surgical patients cannot be weaned from extracorporeal circulation in spite of adequate volume loading, the use of inotropic support, and initiation of intraaortic balloon pumping. In these cases, ventricular assist devices (VAD) can mechanically aid the failing heart and reverse the low output state. The concept of mechanical support for the failing left ventricle was first proposed by Clauss et al. in 1961. By 1968, Kantrowitz and associates had developed and refined the first intraaortic balloon pump (IABP). Through the efforts of Moulopolous and others, this device evolved into the present-day intraaortic balloon pump (IABP). Clinical evidence for the efficacy of left ventricular assist devices (LVAD) remained questionable until 1980, when the National Heart, Blood and Lung Institute evaluated short-term LVADs by comparing various types of mechanical aids. This report focused attention primarily on the failing left ventricle (LV). As the use of inotropic support, intraaortic balloon pumping, and LVADs improved, a small group of patients emerged who could not be separated from extracorporeal circulation due to a failing right ventricle. The failing right ventricle emerged as a unique clinical entity similar to postcardiotomy left ventricular failure that also benefited from mechanical cardiac assistance. Current therapy at major centers incorporating mechanical assist devices is based on the premise that the low output state will allow the failing heart to recover from a reversible injury. The frequent occurrence of postcardiotomy ischemia may be due to several factors such as poor myocardial protection, overdistension of the LV, emboli, coronary spasm or technical problems. Whatever the etiology, the end product of cardiac failure is a demand for oxygen consumption that cannot be met, thus leading to cardiac demise.
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PMID:Mechanical support for postcardiotomy heart failure. 298 17

From 1979 through 1986, 90 patients required intraaortic balloon pumping (IABP) due to low cardiac output complicating open heart surgery. Preoperatively, functional class III or IV was present in 92%; in patients with coronary artery disease (n = 54), three-vessel or left main disease was found in 72%; patients with valvular disease (n = 37) generally had multiple surgical procedures or valve re-replacement performed. Intra-IABP mortality was 49% (n = 44) and 30-day mortality 61% (n = 55). The latter figure decreased from 75% in 1979-81 to 53% in 1985-86. Cumulative 5-year survival was 22%. Logistic regression analysis identified as independent predictors of 30 day mortality the necessity for adjuvant treatment with the more powerful "pressure drugs" isoprenaline/noradrenaline, number of DC-defibrillations, functional classes III-IV, and chronic left ventricular failure. Different combinations of these risk factors identified different patient groups with 30-day mortalities ranging from 100% to 0%. The risk factors reflected both acute cardiac failure probably due to severe ischemia and chronic failure due to advanced primary disease. Taking the high-risk composition of the material into account, a 5-year survival of 22% cannot be regarded as discouraging. Continued employment of IABP treatment in open heart surgery, using an aggressive approach coupled with individualized inotropic support, seems justified.
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PMID:Intraaortic balloon pumping in the treatment of low cardiac output following open heart surgery--immediate results and long-term prognosis. 323 33

The 1st myocardial infarction requires the identification of patients who are at high risk of malignant ventricular arrhythmias. Our study group included 55 consecutive patients (age less than 70): all had non-invasive "signal averaging" recording and 24 hour dynamic electrocardiogram at the post-acute phase of their 1st myocardial infarction (MI) and 3 months later. Wall motion abnormalities were evaluated in each patient but two. 24 randomized patients (without documented sustained ventricular tachycardia) underwent right programmed ventricular stimulation at the 3rd month after MI and pathological repetitive responses were evaluated (Table III); they were hemodynamically stable and without persistent ischemia. Late potentials have been compared to spontaneous and induced ventricular arrhythmias, wall motion abnormalities (Table II) and two-year follow-up (Table VI), in order to identify predictive markers of sudden death or malignant arrhythmias. Ventricular late potentials were identified in 28 patients (51%) 4-8 days after MI: mean duration was equal to 75 +/- 33 msec; they did not show any relationship to the site (Table I) and to the extension of necrosis (Table II). Ventricular late potentials had no significant association with myocardial dyskinesia (Table II) while their association with complex ventricular arrhythmias, detected on Holter monitoring within 8 days after MI, and with the induction of repetitive ventricular responses (greater than or equal to 2 complexes) showed significant correlations (respectively p = 0.02; p = 0.01). In regard of the recognition of spontaneous ventricular tachycardia (greater than or equal to 3 complexes) in the follow-up, the detection of late potentials showed 75% sensibility with predictive value equal to 32% (Table V); the combination of late potentials and ventricular dyskinesia exhibited the highest specificity (88%) and predictive value (54%). By the end of follow-up there had been 6 cardiac deaths (2 sudden, 4 from left ventricular failure): late potentials longer than 75 msec were recorded in all patients who had cardiac death; in the post acute phase of MI repetitive ventricular arrhythmias were detected in only 1 of the 2 case of sudden cardiac death and in none of the patients who developed sustained ventricular tachycardia in the follow-up (Table VI). Myocardial dyskinesia was present in each patient who developed non sudden cardiac death (Table VI).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Late potentials, myocardial kinetics and ventricular vulnerability as markers of sudden death after myocardial infarct]. 372 Nov 3

The paper presents an overview of the recent diagnostic and therapeutic feasibilities in acute coronary heart disease. In unstable angina the leading symptoms are new onset or increasing anginal pain or resting pain as well as ST-T-changes in the ecg without a rise in enzymes. Coronary arteriography shows double or triple vessel disease (70%), a left main stenosis (10 to 15%) or normal coronary arteries (10 to 15%). The treatment of unstable angina in the CCU consists of Nitroglycerin-infusion together with calcium channel blockers and/or betablockers. With this regimen, 80% of patients may be stabilized within 24 to 48 hours. Thereafter coronary arteriography is performed to settle the further therapeutic regimen (PTCA, CABG, medical therapy). Acute myocardial infarction is characterized by persisting (more than 30 min) pain, ST-T-changes in the ecg with or without development of Q-waves indicating irreversible myocardial damage. Angiographically, usually a subtotal or total occlusion of the corresponding artery is found. Aims of therapy in acute myocardial infarction is-besides treatment of complications like arrhythmias and left ventricular failure-reperfusion of the myocardium with reopening of the occluded vessels by intracoronary or systemic thrombolysis. Recently, also clot-specific streptokinase derivates and plasminogen activators are used with fewer bleeding complications. After recanalization of the vessel a persisting stenosis should be relieved either by PTCA or CABG to avoid reocclusion. However, these active forms of treatment can only be performed, if the patient reaches the hospital within 4 to 6 hours after the onset of ischemia.
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PMID:[Acute coronary heart disease. Current status of diagnostic and therapeutic possibilities in the intensive care station]. 372 2


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