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

A patient was admitted because of an acute myocardial infarction which evolved with heart failure and postinfarction angina. A pattern consistent with dynamic left ventricular outflow obstruction was found. It disappeared after coronary angioplasty was performed on the vessel responsible for the ischemia.
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PMID:Acute myocardial ischemia resulting in dynamic obstruction to the left ventricular outflow relieved by successful angioplasty. 145 72

In untreated essential hypertension cardiovascular structural changes will develop after some time. In arteries and arterioles, thickening and reduced compliance of the vascular wall is noted and in the left ventricle, myocardial hypertrophy. Both types of changes will enhance the risk of ischemia and of developing cardiac complications, i.e. coronary heart disease, myocardial infarction and heart failure. Methods for measurement of vascular and cardiac hypertrophy are reviewed and the value of echo-cardiographic evaluation of the hypertensive patient is stressed.
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PMID:[Cardiovascular changes in arterial hypertension]. 146 23

Rapid ventricular pacing (RVP) is used as an experimental model of congestive heart failure (CHF). The purpose of this study was to determine the energy status of the dog myocardium after the development of CHF via chronic RVP. The myocardium had a significantly lower (P < 0.05) energy charge (EC) during CHF (0.63 +/- 0.01) than in sham-operated controls (0.82 +/- 0.02). This was due to significant differences in concentrations in ATP (-48%), ADP (29%), and AMP (275%) in the RVP group. However, the total adenine nucleotide pool was not different between groups. Myocardial lactate concentration was also similar. Glycogen was significantly lower (P < 0.05) by 20% at peak CHF. The adenine nucleotides were similar among the different myocardial layers (endo-, mid-, and epicardium). The administration of enalapril (an inhibitor of angiotension-converting enzyme) to decrease vascular resistance had no effect on the myocardial energy status of CHF dogs. These findings suggest that the lower EC in CHF animals is not the result of subendocardial ischemia. Also, lower EC is not associated with endogenous glycogen depletion or increased lactate concentration. The energy status of the myocardium in RVP-induced CHF is unlike that seen in ischemia-induced heart failure. This suggests that CHF in RVP is not vascular in origin.
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PMID:Energy status of the rapidly paced canine myocardium in congestive heart failure. 149 Sep 44

The organic nitrates have remarkably diverse actions that are or should be beneficial in patients with ischemic heart disease. These drugs are effective in all the important ischemic syndromes. Preliminary data in patients with acute infarction suggest that the drugs may be truly cardioprotective, resulting in improved mortality. This review has not discussed the role of nitrates in congestive heart failure or LV dysfunction, a subject of great importance. The nitrates are useful adjunctive agents in these syndromes, and the two VeHfT trials support the concept that long-term nitrate administration, in conjunction with hydralazine, may favorably alter the natural history of heart failure. This cardioprotective effect is similar to that suggested for the post-MI patient. The data are not strong enough for definitive conclusions at this time. The clinical benefits of nitrates in decreasing subjective (angina) and objective indices of ischemia in stable and unstable angina, as well as limited data in asymptomatic myocardial ischemia, are unequivocal and are as favorable as those for beta blockers or calcium antagonists. Tolerance is an important problem that unfavorably influences the potential benefits of nitrate therapy. I believe that this problem can be avoided with well-designed dosing regimens. Current research into endothelial biology in health and disease has further supported a physiologic role for the organic nitrates in patients with ischemic heart disease. The nitrate-platelet story, while controversial, is promising and offers another positive rationale for nitrate administration. The concept of nitrates replenishing disordered EDRF release or action is an exciting one. Physicians should feel fortunate to have such a remarkable group of drugs available for their patients.
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PMID:Use of nitrates in ischemic heart disease. 151 14

The authors report a case of acute cardiac failure linked to 5 fluoro-uracil. The toxicity seen most commonly involves ischemia. The pathophysiological mechanisms are discussed as well as the role played by pharmacokinetic characteristics in the occurrence of adverse reactions. 5 fluoro-uracil (5 FU) is a compound widely used in the treatment of ENT, breast and gastrointestinal carcinomas. The finding of dose-effect relationship may lead the clinician to use different modes of administration. Continuous administration at high dose 3 g/m2/day from D1 to D5) in combination or not with cisplatin, or continuously at low dose (300 mg/m2/day from D1 to D31) can reduce hematopoietic toxicity but, in contrast, increases gastrointestinal toxicity.
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PMID:[A case of acute cardiac insufficiency caused by 5-fluorouracil]. 151 65

Left ventricular hypertrophy (LVH) constitutes a powerful independent risk factor in hypertensive heart disease. Although initially the wall stress, i.e., left ventricular afterload, remains normal, the coronary reserve is diminished due to disturbances in the microcirculation. This is also shown in the commonly present silent ischemia episodes in Holter monitoring. LVH also causes ventricular dilation and heart failure. Apart from systolic wall stress LVH is modulated by the trophic effects of the sympathetic nervous system and angiotensin II and genetic factors. Long-term antihypertensive treatment must therefore focus on regression of both LVH and the microvascular abnormalities. A step approach for the treatment of the LVH has been recommended on the basis of the experience of this working group with calcium antagonists and ACE inhibitors, whereas the place of beta-blockers is as yet unclear. Preliminary data indicate that coronary flow rescue can also be improved after chronic antihypertensive treatment.
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PMID:Therapeutic effect on left ventricular hypertrophy by different antihypertensive drugs. 153 67

We examined the effect of age on capacity for myocardial hypertrophy, pressure-generating ability and coronary circulation after imposition of pressure-overload. Marked right ventricular and cellular hypertrophy was observed 1 week after pulmonary artery constriction in the developmental phase of rats (2 months of age) and after 3 weeks in the young-adult rats (7 months). In old rats (18 months) similar increases in peak right ventricular pressure did not produce significant hypertrophy even after 3 weeks. The right ventricular hypertrophy at the organ and cell levels in response to pressure-overload decreased with age. In vivo pressure-generating ability, which was determined by maximum isovolumic pressure during pulmonary artery occlusion, correlated with the degree of myocardial hypertrophy in each age group. During the ascending aortic constriction experiment the age-associated diminution in hypertrophic response was also observed in the left ventricle. Coronary dilator capacity, which was determined after brief ischemia in an isolated, blood-perfused, beating but nonworking heart model, was decreased in the presence of myocardial hypertrophy in young-adult rats (7 months) and in the absence of significant myocardial hypertrophy in old rats (18 months). The age-associated diminution in capacity for myocardial hypertrophy, pressure-generating ability and maladaptation in the coronary circulation may explain the higher incidence of heart failure or increased vulnerability of the myocardium to ischemic episodes during hemodynamic stress in aged patients.
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PMID:Aging effects on myocardial hypertrophic response and coronary circulation in pressure-overload. 153 57

Sixteen patients with acute profound heart failure (HF) have been treated with the left ventricular assist device (LVAD), nine of them were successfully weaned from LVAD, and three of them were discharged and survived longer. Decompression of the left ventricle (LV) at the beginning will prevent overextension of impaired myocardium and accelerate scar formation. Gradual increase of LV work will promote the compensation ability of the residual myocardium. We found that continuous LVAD assistance can give time for the impaired heart to recover while maintaining normal circulation. For patients with profound HF which is beyond the limit of intra-aortic balloon pumping's (IABP) capability, LVAD is a more powerful and effective means. Although the heart recovered, many patients later died of multiple organ failure (MOF) which was probably caused by prolonged ischemia before LVAD application. For completely successful recovery from profound HF, diagnosis and deciding to use LVAD should not be delayed. It should be applied before major organs including the heart itself suffer irreversible damage. We have established a systematic therapeutic concept of treating acute HF patients using assisted circulation including LVAD.
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PMID:Treatment of acute profound heart failure by ventricular assist device. 153 71

The risks and benefits of prolonged intraaortic balloon support for the management of refractory congestive heart failure and ischemia were studied in patients with end-stage heart disease who needed support for greater than or equal to 5 days. Fifty-two insertions were performed by the percutaneous femoral route in 49 patients. The duration of insertion ranged from 5 to 46 days (mean 11.3). Clinical outcome including hemodynamic parameters and complications were recorded. Mean systemic arterial pressure did not change with balloon insertion (74 +/- 19 vs 76 +/- 11 mm Hg; p = not significant). Both the mean pulmonary artery and pulmonary arterial wedge pressures decreased (33 +/- 8 to 26 +/- 9 mm Hg [p less than 0.01], and 25 +/- 8 to 17 +/- 6 mm Hg [p less than 0.01], respectively). Over time, both parameters tended to increase, but remained significantly less than those before insertion. Cardiac index increased from 1.6 +/- 0.4 to 2.2 +/- 0.5 liters/min/m2 on insertion and continued to increase to 2.7 +/- 0.5 liters/min/m2 (p less than 0.01) before removal. Definite balloon catheter infection developed in 7 patients, and hemorrhage occurred in an additional 7. Eleven patients had vascular compromise, with loss of pulse in 6, thrombosis of the femoral artery in 1, and pseudoaneurysm in 2. Lacerated femoral artery occurred in 1 patient, and mesenteric artery thrombosis in another. Twenty patients died from progressive heart failure and multiorgan system failure, and 19 survived to receive left ventricular assist device and heart transplantation. Only 10 patients were weaned off the balloon. In conclusion, prolonged intraaortic balloon pump support may be successfully used in end-stage heart disease.
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PMID:Outcome and complications of prolonged intraaortic balloon counterpulsation in cardiac patients. 155 26

The records of 598 patients undergoing a thoracic surgical procedure for lung cancer from 1975 through 1989 were reviewed for occurrence of cardiac arrhythmias and myocardial ischemic events. Atrial tachycardias occurred in 16% (94/598); atrial fibrillation was preponderant (87%), followed by supraventricular tachycardia and atrial flutter. Patients with recurrent episodes of dysrhythmias had a significantly higher mortality rate than those without episodes or with a single episode only (17% versus 2.4%; p less than 0.01). Transient ischemic electrocardiographic changes were documented in 23 patients (3.8%) and myocardial infarction in 7 (1.2%). An abnormal preoperative exercise test result and intraoperative hypotension were strongly associated with both dysrhythmia and ischemia (p less than 0.01). Pneumonectomy, ischemic changes on the electrocardiogram, and cardiac enlargement were also associated with arrhythmias (p less than 0.01). A weaker association (p less than 0.05) was found between postoperative arrhythmias and old myocardial infarction (greater than 6 months), arterial hypertension, and heart failure. Pulmonary function had no predictive value in this respect. A history of angina or old myocardial infarction was predictive of transient postoperative myocardial ischemia but not myocardial infarction. Despite improved anesthetic and monitoring techniques and more frequent use of the intensive care unit postoperatively in the last decade, the incidence of arrhythmias after thoracotomy has not decreased. More effective prevention is needed, particularly for patients with defined preoperative and perioperative risk factors.
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PMID:Cardiac arrhythmias and myocardial ischemia after thoracotomy for lung cancer. 155 74


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