Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with coronary artery disease and normal or near-normal left ventricular function were studied at rest and during atrial pacing until the occurrence of angina (12 patients) before and during infusion of dobutamine (3.80 +/- 0.45 micrograms/kg/min). At rest, during the infusion, three patients developed chest pain, mean ST segment depression increased from 0.02 to 0.08 mV (p less than .001), and myocardial lactate extraction fell from +17.5% to -1.4% (p less than .05). These ischemic changes were associated with significant increases in arterial systolic pressure (134 to 149 mm Hg), heart rate (79 to 91 beats/min), coronary sinus flow (89 to 113 ml/min), and myocardial oxygen consumption (10.8 to 13.5 cc/min). In contrast, during atrial pacing, dobutamine did not reduce the pacing threshold or further increase myocardial oxygen consumption or ST segment changes; however, arterial mean and diastolic pressures were significantly lower with pacing during dobutamine infusion compared with control pacing. In the absence of heart failure, dobutamine in low doses can cause myocardial ischemia in patients with coronary artery disease. The absence of increased ischemia from dobutamine during pacing may reflect reversal of pacing-induced ventricular dysfunction.
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PMID:Effects of low-dose dobutamine on coronary hemodynamics, myocardial metabolism, and anginal threshold in patients with coronary artery disease. 661 88

Chronic therapy with propranolol has been shown to reduce the incidence of sudden death in patients with hypertrophic cardiomyopathy (HCM). However, the long-term effect of beta blockade on exercise capacity has not been studied adequately. Therefore, 32 patients with HCM (21 men), mean age of 47 years (range = 14 to 80 years), were evaluated for dyspnea and chest pain and underwent stress testing (ST) prior to therapy. At entry, ST was contraindicated in four patients, because of heart failure (three patients) and sustained supraventricular tachycardia (one patient). The remaining patients completed 4.9 +/- 3.2 min (mean +/- S.D.) of the Bruce protocol with a functional aerobic capacity (FAC) of 51 +/- 28%. All were placed on propranolol, unless a beta blocker with other characteristics was indicated. Dosage was adjusted to achieve a standing heart rate of 60 beats/min unless adverse effects occurred. At last follow-up, 25 patients were receiving 501 +/- 147 mg propranolol/day while the remainder received nadolol or metoprolol. On the most recent ST, patients exercised 6.6 +/- 3.1 min (38% increase), while mean FAC increased by 24% (both P less than 0.05). The FAC improved by more than 15% in 21, by less than 15% in five, was unchanged in five and was worse in only one, a noncompliant patient. The 21 patients with an FAC increment much greater than 15% exercised longer at entry than the remaining 11 (6.6 +/- 3.3 vs 3.9 +/- 2.8 minutes, P less than 0.05). The mean peak ST blood pressure-heart rate product of the group decreased from 26 550 to 17 898 (P less than 0.05), while the symptom scores of dyspnea and chest pain declined from 2.2 +/- 0.8 to 0.8 +/- 0.7 and from 1.4 +/- 1.0 to 0.3 +/- 0.8, respectively (both P less than 0.001). We conclude that beta blockade produces sustained improvement in exercise capacity. Improvement was greatest in those with the least initial impairment, and appears to be related to a reduction in blood pressure-heart rate product.
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PMID:Long-term medical management of hypertrophic cardiomyopathy: usefulness of propranolol. 668 31

We evaluated the effects of intravenous verapamil, a calcium antagonist, on hemodynamics and regional left ventricular (LV) performance in patients with acute myocardial infarction (AMI). Twenty patients having uncomplicated infarction or moderate heart failure were randomized to receive either verapamil or placebo and were studied a mean of 12 hours after onset of symptoms. Verapamil, 7.5 mg intravenously, acutely reduced systolic arterial pressure (p less than 0.0005), systemic vascular resistance, and LV stroke work (p less than 0.005) and rate-pressure product (p less than 0.05); the heart rate did not alter. The Frank-Starling relationship by Swan-Ganz catheter did not change for 1 hour. Segmental wall motion amplitudes were recorded from eight standardized segments around the left ventricle by a multidirectional M-mode echocardiographic technique. The systolic wall motion of the uninvolved LV segments and LV cavity size did not change after verapamil. Verapamil improved mechanical performance in the ischemic segments (p less than 0.005). Therefore, the overall regional contractile function of the left ventricle improved as well (by 11% to 13%, p less than 0.05). This echocardiographic improvement continued after the acute vasodilatory response of intravenous verapamil subsided and was preserved for 1 week, the patients having had oral verapamil, 240 mg daily. Chest pain was relieved in five of the six patients having ongoing slight pain before verapamil injection. No sequential hemodynamic or echocardiographic changes occurred in the placebo-treated patients. Thus, in patients with uncomplicated AMI, verapamil improve contractile function of the acutely ischemic LV segments by hemodynamic unloading and/or by direct myocardial effect, without manifest depression of the uninvolved myocardium.
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PMID:Effects of verapamil in patients with acute myocardial infarction: hemodynamics and function of normal and ischemic left ventricular myocardium. 669 58

Treatment with captopril has proved effective in some patients with resistant heart failure. Since cardiac output responses to captopril treatment are generally small, we infused the positive inotropic agent dobutamine in six patients already receiving captopril to determine whether cardiac output could be augmented without concomitantly increasing myocardial oxygen demands. At low infusion rates of dobutamine (2.5 and 5 microgram/kg per min), a substantial rise in cardiac output was observed yet myocardial oxygen uptake remained well below baseline (pre-captopril/dobutamine) levels. At higher rates of infusion (10 and 20 microgram/kg per min) the rise in cardiac output was accompanied by a pronounced increase in myocardial oxygen uptake, and the appearance of chest pain or multifocal ventricular extrasystoles in three patients. These data indicate that captopril treatment combined with low infusion rates of dobutamine can augment cardiac output in the short term, without increasing myocardial oxygen demand.
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PMID:Haemodynamic effects of dobutamine in patients with congestive heart failure receiving captopril. 703 56

Twelve subjects without clinical or hemodynamic heart failure, admitted for a first untreated anterior transmural myocardial infarction, were evaluated within the first 24 hours after the onset of symptoms. Pulmonary angiography was performed while a right ventricular extrastimulus was delivered every fourth beat at 50% of the RR interval to systematically analyze the basal and the postextrasystolic left ventricular frames. Left ventriculograms were quantitatively processed to determine the ejection fraction (EF) and the percentage of the end-diastolic circumference showing hypokinetic (%HK) or akinetic (%AK) areas. Left ventricular angiography was performed 1 month later in all cases at the same paced atrial heart rate to compare this final angiogram to the basal and the electrically induced postextrasystolic initial beats. During the 1-month period of the study none of these subjects had complications such as recurrent chest pain, heart failure or rhythm disturbances, and no drug administration was necessary. Comparing the basal cycle of the initial angiogram and the final cycle, a poor correlation was found between the corresponding values of EF (r = 0.34), %HK (r = 0.38) and %AK (r = 0.48). The correlations were much better when a comparison was made between the postextrasystolic cycle of the initial angiogram and the final cycle (EF, r = 0.84; %HK, r = 0.96; %AK, r = 0.95). These results indicate that, from the first day after a TMI, the analysis of the postextrasystolic frame allows accurate estimation of the final left ventricular function and regional wall motion abnormalities. Postextrasystolic potentiation may be useful in the acute state of transmural infarction to discriminate potentially reversible ischemic from definitely jeopardized areas.
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PMID:Detection of residual myocardial function in acute transmural infarction using postextrasystolic potentiation. A computerized angiographic study. 723 24

The hemodynamic monitoring of acute myocardial infarctions has been carried out in patients less than 75 y.o. who showed: a) extensive anterior myocardial infarction; b) inferior myocardial infarction and ST segment depression of the anterior chest leads; c) acute myocardial infarction and cardiac failure. The hemodynamic measurement were carried out at the 12 hours (mean) from the beginning of chest pain on 65 patients who suffered the first myocardial infarction and were protracted to 60 hours (mean). The hemodynamic findings were classified according to the relationship between the stroke work index of the left ventricle (LVSWI) and the mean pulmonary artery pressure (MPAP) as following: normals: 6 pts; hypovolemia: 15 pts; reduced compliance: 2 pts; mild LV failure: 19 pts; severe LV failure or shock: 23 pts. 35 pts have carried out a complete rehabilitation programme has shown an inverse linear relationship to the MPAP of the first recording in CCU. The incidence of death was 29% one year after the myocardial infarction and showed a significant relationship to the hemodynamic findings. The LVSWI resulted more sensitive than MPAP; 90% of patients who showed a LVSWI less than 20 gmb/m2 died.
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PMID:[Correlations among the haemodynamic effects in acute myocardial infarction. Function evaluation and prognosis 12 months later (author's transl)]. 732 21

We studied 67 patients with tachycardia and chest pain admitted with suspected myocardial infarction; 29 had myocardial infarction (20 transmural, nine subendocardial) with elevated MB creatine kinase (CK) activity, as well as elevated total CK and lactate dehydrogenase (LDH) levels. However, hydroxybutyric dehydrogenase and SGOT activity remained normal in three and four patients, respectively. Despite abnormal ECGs in 84% and typical chest pain in 54%, 38 patients had normal MB CK activity. However, 15 of them had elevated MM CK levels, presumably due to release from skeletal muscle. In total, 29 patients had elevated activity of MM, CK, LDH, or SGOT, but 72% of these patients had cardiac failure, hypotension, or skeletal muscle trauma due to cardioversion. Eleven patients with normal MB CK had elevated hydroxybutyric dehydrogenase activity. Despite elevated activity of other enzymes, MB CK remained normal. Thus, elevated plasma MB CK activity appears to remain a good diagnostic marker of myocardial necrosis in patients with tachyarrhythmias.
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PMID:Plasma MB creatine kinase activity and other conventional enzymes. Comparison in patients with chest pain and tachyarrhythmias. 736 51

The ability to perform bedside examinations in acutely ill patients, the sensitivity of the technique and the accuracy of serial examinations have led to increasing use of echocardiography in the intensive care setting. In addition to diagnostic information, the procedure provides the clinician with objective reproducible data for noninvasive evaluation of follow-up and therapeutic action. It provides an important approach to the patient with cardiac enlargement and congestive heart failure. In the patient with chest pain it may detect a cause of ischemia other than coronary artery obstruction and in the presence of unquestionable coronary artery disease it provides information towards early recognition and follow-up of complications. In acute left-sided heart failure it helps in the delineation of conditions amenable to specific therapeutic interventions. Echocardiograpy may point to the origin of systemic emboli by detecting mitral and valvular vegetations in infectious endocarditis, mitral stenosis and in rare cases of atrial myxoma. It may accelerate decisions for invasive procedures.
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PMID:[Significance of echocardiography in monitoring blood circulation]. 739 7

A series of 89 surgical patients (111 operations) with preoperative myocardial infarction (MI) was analysed for factors predisposing to the development of a postoperative reinfarction. Six of them suffered postoperative MI, and three of these patients died. In the statistical analysis the following risk factors emerged: age over 60 years, anaemia, hypertension, and the fact that the previous MI had been posterior. Abdominal operations were more dangerous concerning reinfarction than other operations. In the other series of 11 deceased patients with postoperative reinfarction collected from the autopsy material, about the same risk factors were found. The most important factor seemed to be hypotension, which complicated the surgery. All 11 patients had arrhythmias in their preoperative electrocardiogram. Previously treated heart failure was present in five of these patients. Postoperative symptoms analysed in the first series suggest that if a patient with preoperative MI has arrhythmias, hypotension, dyspnoea, diffuse unlocalized pain or chest pain after surgery, he is very likely to have a reinfarction.
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PMID:Risk factors in surgical patients with verified preoperative myocardial infarction. 744 39

A young Protugese man, who had never travelled outside of Europe, was found to have a bacterial complication of a fibroplastic endocarditis. The onset was by a spontaneous chest pain, associated with a posterolatero-apical subepicardial ischemia and giant T waves in V3, V4, and calcification in the apex of the heart on radiography. Diagnosis was confirmed by intracardiac explorations: ventricular telediastolic pressures were increased; the lower border of the right ventricle was smooth, the left ventricle had a globular appearance with a smooth anterior border, the apex appearing to be completely excluded; coronarography was normal. Histological examination confirmed the presence of fibrosis. Anticoagulant treatment was started. Four months after the onset of the disease, a high fever, an apical systolic murmur, and nine positive blood cultures for a streptococcus mitis, suggested the development of a bacterial endocarditis, though no direct evidence was discovered. Improvement occurred after appropriate antibiotic therapy, and the anticoagulants were continued. Cardiac ultrasonography recordings were normal following this episode. This case-report is of two-fold interest: on the one hand it represents an early form of fibroplastic endocarditis, diagnosed by intracardiac exploration, and on the other hand it emphasizes the rare nature of bacterial complications of this affection. Authors differ in their evaluation of the frequency of chest pain, but their inaugural and isolated nature are rarely described. In most cases the presence of the disease is revealed by a progressive cardiac insufficiency. A very positive factor is the presence of calcifications, and the absence of an eosinophilia does not exclude the diagnosis. Electrical anomalies of the ischemic type are possible, but are rarely isolated findings, and the giant appearance of the T waves in this case is rather atypical. Bacterial complications are rare, and are only reported in 12 of the 218 cases described in the published literature. They are rarely diagnosed during the life of the patient (1 case only). The infection affects the cords, the valves, the thrombus, or the fibrosis itself.
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PMID:[Bacterial endocardiitis complicating fibroplastic endocarditis: a case report (author's transl)]. 746 43


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