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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 85 patients (68 with coronary heart disease in the presence of effort angina of various functional classes (a major group) and 17 with neurocirculatory++ dystonia and cardialgic syndrome (a control group)) were examined. Heart failure severity and blood flow distribution in the functioning myocardial areas were evaluated in transient ischemia induced by atrial pacing. Three levels of coronary venous blood flow were defined in patients with coronary heart disease. A relationship between the coronary blood flow, disease history duration, and coronary blood flow changes was examined in cardioselective exercise.
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PMID:[Status of coronary venous blood flow in patients with ischemic heart disease in myocardial ischemia induced by the atrial stimulation test]. 189 38

Recent trials of myocardial reperfusion using single-agent thrombolytic therapy and sequential cardiac catheterization have supported a conservative approach to the patient with acute myocardial infarction. To evaluate combination thrombolytic therapy and the role of a previously untested strategy for the aggressive use of cardiac catheterization, we performed a multicenter clinical trial with a 3 x 2 factorial design in which 575 patients were randomly allocated to one of three drug regimens--tissue-type plasminogen activator (t-PA) (n = 191), urokinase (n = 190), or both (n = 194) - and one of two catheterization strategies--immediate catheterization with angioplasty for failed thrombolysis (n = 287) or deferred predischarge catheterization on days 5-10 (n = 288). Patients with contraindications to thrombolytic therapy, cardiogenic shock, or age of more than 75 years were excluded. Global left ventricular ejection fraction was well preserved and almost identical at predischarge catheterization (54%), regardless of the catheterization or thrombolytic strategy used (p = 0.98). Combination thrombolytic therapy was associated with a less complicated clinical course, most clearly documented by a lower rate of reocclusion (2%) compared with urokinase (7%) and t-PA (12%) (p = 0.04) and a lower rate of recurrent ischemia (25%) compared with urokinase (35%) and t-PA (31%). When a composite clinical end point (e.g., death, stroke, reinfarction, reocclusion, heart failure, or recurrent ischemia) was examined, combination thrombolytic therapy was associated with greater freedom from any adverse event (68%) compared with either single agent (urokinase, 55%; t-PA, 60%) (p = 0.04) and with a less complicated clinical course when the composite clinical end points were ranked according to clinical severity (p = 0.024). Early patency rates were greater with combination therapy, although predischarge patency rates after considering interventions to maintain patency were similar among drug regimens. No difference in bleeding complication rates was observed with any thrombolytic regimen. The aggressive catheterization strategy led to an overall early patency rate of 96% and a predischarge patency rate of 94% compared with a 90% predischarge patency in the conservative strategy (p = 0.065). The aggressive strategy improved regional wall motion in the infarct region (-2.16 SDs/chord) compared with deferred catheterization (-2.49 SDs/chord) (p = 0.004). More patients treated with the aggressive strategy were free from adverse outcomes (67% versus 55% in the conservative strategy, p = 0.004), and the clinical course was less complicated when the adverse outcomes were ranked according to severity (p = 0.016). No significant increase in use of blood products resulted from the aggressive strategy.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evaluation of combination thrombolytic therapy and timing of cardiac catheterization in acute myocardial infarction. Results of thrombolysis and angioplasty in myocardial infarction--phase 5 randomized trial. TAMI Study Group. 202 33

The relationship between myocardial ischemia and biochemical changes has been well documented. For example, hyperlipidemia is one of the largest risk factors for the development of coronary artery disease. Decreased coronary blood flow produces various changes in cardiac metabolism, which cause severe cardiac function abnormalities, including heart failure and arrhythmias. Many biochemical markers have been used for both diagnosis and evaluation of the severity of myocardial infarction. In this symposium the speakers have discussed: 1) the relationship between the changes in the ionic environments in the intra- and extra-cellular spaces and the genesis of cardiac arrhythmias, with special reference to the role of increased intracellular resistance in conduction delay during ischemia (Dr. Takao Fujino), 2) metabolic basis of ECG abnormalities in ischemic heart disease and the role of intra-coronary ECG recordings in the evaluation of cardiac ischemia (Dr. Tetsunori Saikawa), and 3) biochemical changes associated with exercise and other stresses, with special reference to the roles of increased catecholamines and decreased blood fluidity in the genesis of cardiac abnormalities (Dr. Takehiko Fujino). Prof. Takeshi Kanno gave a special lecture entitled "Approaches from clinical laboratory to hereditary variants". He showed an excellent model of approach from clinical laboratory medicine to detect important biochemical abnormalities which may be overlooked by routine daily analyses in the clinical laboratory.
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PMID:[Cardiac function abnormalities and biochemical changes in myocardial ischemia]. 192 Aug 72

Endomyocardial biopsy (EMB) is a valuable diagnostic procedure for rejection surveillance in heart allograft recipients and is widely used for evaluation of native heart disease. However, the spectrum and incidence of diagnoses encountered on a heart failure/cardiac transplant service deserve clarification. Of 2300 consecutive EMBs performed during a 2.5-yr period, 79.9% had been performed for rejection surveillance in heart allograft recipients. Of these, 1281 (69.7%) were negative for rejection; 536 (29.1%) were positive (18.9% mild, 9.7% moderate, 0.5% severe); 21 (1.1%) were not interpretable due to insufficient samples. Endocardial lymphocytic infiltrates ("Quilty" effect) were present in 86 (4.7%), ischemia in 12 (0.7%), myocardial calcification in five (0.3%), foreign body giant cells in two (0.1%), valvular tissue in two (0.1%), and liver tissue in one (0.05%). Of the 20.1% of EMBs performed in patients with native heart disease, 298 (64.5%) were abnormal. A total of 239 (51.7%) had myocyte hypertrophy and/or fibrosis, while 37 (8.0%) had active or ongoing myocarditis, two of which were of the giant cell type. Other diagnoses included anthracycline cardiotoxicity in 11 (2.4%), amyloidosis in five (1.1%), hemochromatosis in two (0.4%), healed infarct in two (0.4%), scleroderma in one (0.2%), and foreign body granuloma in one (0.2%). A total of 159 (34.4%) samples had no diagnostic abnormalities; five (1.1%) were insufficient samples. As the number of EMBs performed grows, pathologists must develop expertise in the detection of morphological features pertaining to various cardiac conditions which may have similar clinical presentations.
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PMID:Pathological findings in 2300 consecutive endomyocardial biopsies. 192 75

Positive inotropy requires a rise in myocardial oxygen consumption (MVO2); as far as PDE-III-inhibitors' beneficial hemodynamic effects, increases in contractility are controversial, in part probably because accurate proving is rather tedious. The clinician, however, requires a clear concept of whether or not enoximone (EN), for example, carries the risk of myocardial ischemia when used in patients with coronary artery disease. Using the analysis of pressure-volume relations, we recently established contractility-increasing as a partial effect of EN. There are indications suggesting that the inotropy-induced added increase in MVO2 of the PDE-III-inhibitor drugs could be compensated for by the simultaneous vasodilation and changes in compliance, so that as a net effect an unchanged MVO2 might result. Since, on the other hand, PDE-III-inhibitor drugs have been said to generate antiischemic properties, further clinical investigations with EN clearly seemed indicated and they are the subject of the present report: In five patient groups with stabile angina (AP) studied the following parameters and methods, respectively, were used for the evaluation of EN-induced changes of the anginal threshold: exercise, using pacing and ergometry; PA- and PC-pressure measurements; MVO2, indirectly assessed; hemodynamic profile and regional wall motion as assessed in the immediate post pacing phase; ST- T-segment evaluation; thalium-201 perfusion scintigraphy; myocardial perfusion, indirectly assessed. Lack of EN-induced AP (ischemia) and an increased AP threshold indicated that the drug can be used safety in patients with heart failure, including that due to coronary artery disease.
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PMID:[Effects of the phosphodiesterase III inhibitor in ischemic heart disease]. 192 97

Seventy-nine patients with ischemic mitral regurgitation were followed up for a period of 20 +/- 8 months. The risk of death increased with age and cardiac failure at the time of inclusion. The risk of cardiac events increased with these factors and also with raised serum creatinine and decreased echocardiographic fractional shortening. The global 2 year survival was 72.8% and survival without a further cardiac event was 48.7%. Surgery and angioplasty increased global survival and freedom from cardiac events of patients with severe regurgitation (74.9% and 68.8% versus 59.4% and 46.1% for medical therapy alone). The functional improvement was also greater in patients undergoing surgery or angioplasty (80% of patients in NYHA Stage I versus 53.8% in the medical group). Angioplasty was only performed in cases of paroxysmal mitral regurgitation by reversible papillary muscle ischemia. Surgery (coronary bypass usually associated with mitral valve replacement) was associated with better results than medical therapy alone in permanent mitral regurgitation by papillary muscle dysfunction or rupture. Despite a high immediate mortality, this option should be considered rapidly in cases of severe ischemic mitral regurgitation with pulmonary oedema.
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PMID:[Prognosis of ischemic mitral valve insufficiency]. 192 8

Between 50 and 70% of patients with heart failure die suddenly and unexpectedly before they have deteriorated to New York Heart Association class IV symptoms. It has long been known that ventricular ectopy predicts sudden cardiac death in coronary heart disease, and this has also been shown in dilated cardiomyopathy. It is less certain whether antiarrhythmic drugs reduce this risk and improve prognosis. Supraventricular arrhythmias frequently develop in heart failure of all causes. They nearly always cause symptoms, and the establishment of atrial fibrillation may mark a permanent deterioration. Except for sustained ventricular tachycardia, ventricular arrhythmias are often occult. Hypokalemia and digitalis toxicity may have been precipitated by diuretics or interaction with antiarrhythmic drugs. In coronary heart failure, arrhythmias may be related to scar tissue or ischemia, which may also be responsible in dilated cardiomyopathy. Use of inotropes and inodilators may precipitate arrhythmias, whereas drugs that conserve energy or potassium, such as beta blockers and angiotensin-converting enzyme inhibitors, may prevent them. Since suppression of ventricular arrhythmias has not been shown to prevent sudden death or prolong life in patients with heart failure, it may be that such arrhythmias do not directly presage ventricular fibrillation except in so far as they are markers of a poor prognosis with a risk of sudden death. If so, such arrhythmias are most likely to be suppressed by agents that result in improvement of left ventricular function and, through that, prolongation of life.
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PMID:Genesis of arrhythmias in the failing heart and therapeutic implications. 202 Nov 15

Among the clinical manifestations of ischemic heart disease, right coronary artery (RCA) disease offers a wide variety of right and left ventricular ischemic involvement, including prevalent right ventricular dysfunction and severe cardiac failure. Whether the right ventricular impairment is dependent primarily on ischemia of the right ventricle or requires a concomitant left ventricular dysfunction remains debatable. To assess the pathophysiology and clinical relevance of RCA-related ischemia, a systematic study of patients with single RCA disease (either vasospastic angina at rest or typical stable angina) was undertaken by radionuclide ventriculography. A high incidence of ischemia-induced right ventricular dysfunction was observed (93% and 95% in angina at rest and on effort, respectively), either alone or associated with left ventricular impairment. These results were compared with those obtained in a control population with isolated left anterior descending artery disease and either primary or secondary angina pectoris. We infer that the impairment of the right ventricle was related primarily to right ventricular ischemia and that left ventricular dysfunction alone did not cause an important depression of right ventricular systolic function. In conclusion, the clinical manifestations of RCA disease can be protean; the right ventricle can be the target of ischemia, and recognition of its impairment poses diagnostic problems. Radionuclide ventriculography and two-dimensional echocardiography, together with stressors of coronary flow reserve, are reliable techniques for assessing RCA-related ischemia.
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PMID:Right coronary artery disease. Pathophysiology, clinical relevance, and methods for recognition. 202 49

In the majority of patients with intestinal infarction, it is generally agreed that the occlusion of mesenteric arteries or vein is the primary etiologic factor; however, some showed no evidence of thrombosis, embolization or vasculitis as the causative factor. In many patients, this particular type of infarction is the terminal event of the episode. From October 1977 to December 1986, 24 patients with mesenteric infarction were investigated following cardiovascular surgery in our institute. Among them, 15 were diagnosed with organic vascular occlusion; however, the other 9 showed no evidence of thromboembolism or any other organic vascular occlusive lesion of mesenteric vessels and were diagnosed as non-occlusive mesenteric infarctions. All of these patients were in severe cardiac failure (LOS) postoperatively. There was no typical symptom, although abdominal fullness and diarrhea were the major and consistent findings. In blood chemical analysis, the enzymatic levels such as serum GOT, LDH and CPK were significantly elevated and discrepancy between serum GOT and serum GPT was observed. In this clinical situation, it was difficult to establish a correct diagnosis mainly because of the few signs and symptoms present relating to the mesenteric infarction. On the other hand, when the correct diagnosis was made, these patients were too critically ill to be treated conservatively. The outcome of these patients was grave and all of them died which showed 100% of mortality rate. The conservative management did not produce favorable progress, which accelerated LOS and prevented patients from recovering from cardiac failure. The aggressive surgical approach to this particular type of acute mesenteric ischemia might have offered an improved prognosis from these catastrophic events.
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PMID:[Non-occlusive mesenteric infarction following cardiovascular surgery]. 202 11

Postoperative changes in serum myoglobin levels have been studied in 47 patients undergoing open heart surgery. The patients were retrospectively divided into two groups according to the time to peak myoglobin level during reperfusion. In 38 patients, myoglobin levels increased rapidly to a peak within 3 hours after reperfusion, after which it was cleared from the blood (group 1). Contrarily, a rise in myoglobin levels was persistent for 24 hours and its time to peak was greater than 3 hours after reperfusion in nine patients (group 2). There were no differences in preoperative and early reperfusion (within 1 hour of reperfusion) values of myoglobin between the two groups. At 3, 6, and 12 hours of reperfusion, myoglobin levels were significantly greater in group 2: 448 +/- 196 vs 1,149 +/- 900 ng/ml, 359 +/- 172 vs 2,653 +/- 3,179 ng/ml, 184 +/- 95 vs 1,896 +/- 1,387 ng/ml, respectively, p less than 0.0001 in each. The maximum activities of both myoglobin and CK-MB were significantly higher in group 2 (myoglobin-max: 771 +/- 257 vs 3,221 +/- 3,024 ng/ml, p less than 0.0001; CK-MBmax: 107 +/- 60 vs 227 +/- 219 IU/L, p less than 0.005). Five of nine patients in group 2 required post-operative assistance with intra-aortic balloon pumping (p less than 0.0005 compared with one of 38 in group 1) and perioperative myocardial infarction developed in three patients (33.3 percent) in this group (p less than 0.005 compared with 0 percent in group 1). Thus, patients with a delayed peak of serum myoglobin level exhibited detrimental cardiac failure postoperatively. These findings suggest that myocardial injury accelerated by reperfusion following ischemia might progress in these patients.
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PMID:Delayed time to peak serum myoglobin level as an indicator of cardiac dysfunction following open heart surgery. 203 22


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