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

The initiating cause of the first ectopic beat and its precipitation of sustained lethal arrhythmia in acute myocardial ischemia is not clear. Comparable uncertainties surround sudden death in myocardial failure. Progress in control of ventricular fibrillation has been slow, perhaps because diagnosis and treatment have been based on the premise that ischemic biochemical changes solely cause the alterations in electrophysiological behavior. Alternative approaches need exploration. Evidence that mechanical changes can initiate electrophysiological changes by a process sometimes referred to as "mechanoelectric feedback" is accumulating. It operates when any primary mechanical change in ventricular muscle, e.g., contraction produces a change in its electrical properties. Mechanical changes are prevalent in ischemia and cardiac failure. If mechanoelectric feedback operates here, it is not surprising that arrhythmias in some of these pathologies parallel the degree of mechanical myocardial dysfunction rather than electrophysiological changes, independent of etiology. This mechanoelectric feedback system may exist as an intrinsic property of normal myocardium, providing a feedback control of activation processes at both the cellular and gross levels. Its disruption during pathological events produces instability in the system and thus ventricular arrhythmia. This concept provides a new potential avenue for arrhythmia therapy.
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PMID:Myocardial mechanics and arrhythmia. 172 49

Although both asymptomatic ventricular arrhythmias and sudden death are common in patients with chronic heart failure, there is little evidence that patients who have frequent or complex ventricular arrhythmias are at increased risk of sudden death. Two hypotheses may explain the lack of an arrhythmia-sudden death relation in this disorder. First, complex ventricular arrhythmias may be a nonspecific manifestation of a dying left ventricle rather than an indication of a specific arrhythmogenic substrate. In fact, during long-term follow-up, patients with mild heart failure who have nonsustained ventricular tachycardia are more likely to develop clinical progression of the disease rather than sudden death. Second, sudden death may be related to events other than a malignant ventricular arrhythmia. The most common myocardial ischemia, whereas the terminal event in patients with an idiopathic dilated cardiomyopathy is commonly a severe bradyarrhythmia or electromechanical dissociation. Neither outcome can be predicted by a prior history of ventricular arrhythmias on ambulatory electrocardiographic monitoring. If asymptomatic ventricular arrhythmias do not lead to sudden death, then there would appear to be little reason to expect that antiarrhythmic drugs could prevent cardiac arrest in patients with chronic heart failure. This may explain why drugs that suppress ambulatory arrhythmias do not prevent sudden death in these patients, whereas interventions may reduce the risk of unexpected circulatory collapse in this disorder without suppressing ventricular ectopic activity. To make matters more complicated, the desirable actions of antiarrhythmic drugs are attenuated and their negative inotropic and proarrhythmic actions are enhanced in patients with severe cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of relation between ventricular arrhythmias and sudden death in patients with chronic heart failure. 172 5

Little information is available about the incidence of severe adverse outcomes, and even less information is available about the identification and quantification of independent predictors of severe perioperative adverse outcomes. The purpose of this study was to identify and quantitate independent predictors of severe perioperative adverse outcomes in a prospective randomized clinical trial of general anesthesia in 17,201 patients. Twenty-nine prognostic variables for 15 severe outcomes in 847 patients were tested by multiple stepwise logistic regressions from which 20 significant (P less than 0.05) predictors were identified. A history of cardiac failure or myocardial infarction less than or equal to 1 yr; ASA physical status 3 or 4; age greater than 50 yr; cardiovascular, thoracic, abdominal or neurologic surgery; and the study anesthetics were significant predictors of "any severe outcome, including death." There were 17 significant predictors for 10 severe cardiovascular outcomes in 608 patients, including a history of ventricular arrhythmia, hypertension, cardiac failure, myocardial ischemia, myocardial infarction less than or equal to 1 yr or myocardial infarction greater than 1 yr, and smoking; ASA physical status; age; cardiovascular, thoracic, abdominal, eyes-ears-nose-throat/endocrine, neurologic, musculoskeletal, or gynecologic surgery; and the study anesthetics. There were 9 significant predictors for 4 severe respiratory outcomes in 163 patients, including a history of cardiac failure, myocardial ischemia, or chronic obstructive pulmonary disease; obesity; smoking; male gender; ASA physical status; abdominal surgery; and the study anesthetics. Colinearity between related prognostic variables (such as disease and ASA physical status) was assessed using progressively segregated groups of variables in eight stepwise logistic regressions. We conclude that the comprehensive stepwise logistic regression of 29 prognostic variables reported here provides a valid estimate of the risks of severe perioperative outcomes associated with general anesthesia.
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PMID:Multicenter study of general anesthesia. III. Predictors of severe perioperative adverse outcomes. 172 12

Treatment of patients with heart failure due to major ventricular systolic dysfunction should aim not only at symptomatic but also at prognostic improvement. If correction of the underlying problem is not possible, treatment should slow down the progression of cardiac failure and eliminate triggers for sudden cardiac death due to electromechanical dissociation or arrhythmias. In every patient with chronic congestive heart failure screening for myocardial ischemia and complete revascularization is mandatory, if possible. In patients with coronary artery disease and diminished systolic function, beta-blockade may improve prognosis by reducing ischemic events and sudden cardiac death. The incidence of life-threatening arrhythmias in patients with heart failure may be reduced by eliminating facilitating factors like electrolyte disturbances, altered autonomic tone and raised intracardiac pressure rather than by antiarrhythmic medical treatment itself. One of the most important prognostic aspects in treatment is the interference with the development of the cardiomyopathy of overload, uniformly observed in chronic congestive heart failure. Modification of mechanical and neuroendocrine stimuli may postpone myocardial hypertrophy and interstitial hyperplasia as a consequence of altered gene expression. Early treatment with ACE inhibitors and in certain patients with betablockers are the most promising strategies to delay the progression of the disease. In contrast, positive inotropic drugs, including digitalis and phosphodiesterase inhibitors, do not improve prognosis. Calcium antagonists should also be used with restriction, as Verapamil and Diltiazem, but also Nifedipine may adversely affect the outcome in congestive heart failure patients.
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PMID:[Prognostic aspects in the treatment of chronic heart insufficiency]. 173

We prospectively compared the differences in perioperative cardiac ischemic events in 140 patients undergoing major abdominal (n = 53) versus infrainguinal (n = 87) vascular operations. Preoperative dipyridamole thallium cardiac scintigraphy was performed in a subset of 38 of these patients, with treating physicians blinded to the test results. Myocardial ischemia was measured during operation with use of continuous 12-lead electrocardiography (ECG) and transesophageal echocardiography. Continuous two-lead ambulatory ECG (Holter monitoring) was performed before, during, and after operation for 4 days. Outcome events were cardiac death, nonfatal myocardial infarction, unstable angina, ventricular tachycardia, and congestive heart failure. Results of the study indicated that most demographic variables, such as age, hypertension, cigarette smoking, serum cholesterol, were comparable between patients having aortic or infrainguinal arterial operations. However, in the infrainguinal group more patients had diabetes, second vascular operations, angina pectoris, heart failure, dysrhythmias, and used digitalis. Abnormalities in preoperative Holter monitoring, ECGs, and thallium scan abnormalities were equivalent between groups. During operation, whereas Holter and ECG abnormalities were comparable, more patients undergoing aortic procedures suffered ischemia as determined by transesophageal echocardiography (26% vs 10%, p = 0.019). After operation there were 21 (24%) outcome events in patients having infrainguinal bypasses compared with 15 (28%) patients having aortic procedures (p = NS). Ischemia by Holter monitoring (n = 133) occurred after operation in 46 (57%) patients having infrainguinal operations compared with 16 (31%) patients having aortic reconstructions (p = 0.005). Because preoperative cardiac disease and adverse cardiac outcomes occurred with similar or even greater frequency in both groups of patients, we conclude that the risk for postoperative cardiac ischemic events in lower extremity vascular operations is at least as great as for aortic operations.
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PMID:Comparison of cardiac morbidity between aortic and infrainguinal operations. Study of Perioperative Ischemia (SPI) Research Group. 173 96

Ten healthy (aged 28 to 39) and ten heart failure NYHA II (aged 19 to 49) male subjects were prospectively studied under no drugs, under furosemide (40 mg/day), under captopril (150 mg/day) and under their association. Arterial compliance (ml/mmHg) was measured in all subjects at rest and supine. Heart failure etiology was dilated cardiomyopathy or ischemic heart disease without significant regurgitation. Arterial compliance was significantly higher in healthy than in heart failure patients in all studied conditions (p less than 0.001) (healthy = 2.2 + 0.29 vs. heart failure = 0.79 + 0.14). Neither single drug nor their association induced any change in healthy subjects. Arterial compliance progressively increased in heart failure with furosemide, captopril, and their association (no drug = 0.79 + 0.14; furosemide = 0.87 + 0.15; captopril = 0.94 + 0.15 and furosemide + captopril = 0.99 + 0.14). Captopril induced a higher increment than furosemide (p less than 0.001) and their association even a higher increment (p less than 0.001) than any single drug. Thus captopril and/or furosemide increased arterial compliance in heart failure but not in healthy subjects, possibly through changes in arterial wall edema and smooth muscle contraction.
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PMID:Effect of drugs on a noninvasive index of arterial compliance in healthy and heart failure patients. 174 91

Using non-invasive radionuclide techniques, we studied the arterial and venous effects of 0.1 mg/kg oral felodipine in 12 men with heart failure due to ischaemic heart disease aged 37-72 y. All were in New York Heart Association Class II or III, required frusemide 40-120 mg daily and were clinically stable. Felodipine produced significant falls in blood pressure (-19%) and systemic vascular resistance (-39%) with increases in cardiac index (+34%), heart rate (+12%) and left ventricular ejection fraction (from 0.25 to 0.32). Peripheral venous volume fell by 10.6% after felodipine indicating venoconstriction rather than venodilatation and may be caused by an acute sympathetic reflex associated with the increase in heart rate. Our results confirm that felodipine is an arterial vasodilator. The previously observed changes in cardiac filling pressures may simply represent improved ventricular function as a consequence of reduced afterload, not venodilatation.
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PMID:Central and peripheral haemodynamic responses to felodipine in congestive heart failure. 174 53

Preoperative identification of cardiac insufficiency in patients with ischemic heart disease (IHD) has proved essential for the success of surgery on the coronary arteries. To provide for an objective assessment of the contractile function of the myocardium in selecting candidates for surgery among IHD patients with over 70-percent narrowing of one, two, and three coronary arteries, use was made of the central hemodynamics indices in response to the loading test during right heart catheterization with computer-assisted monitoring and mathematical analysis. Two patient groups were distinguished during the hemodynamic loading test: group I showing a high and effective chronotropic reserve (+X) and group II presenting a negative chronotropic reserve (-X). It was established that with equal numbers of narrowed coronary arteries and similar clinical manifestations, the estimates of myocardial contraction may differ which determines indications for surgery and preoperative care.
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PMID:[Detection of cardiac insufficiency by computer-assisted monitoring of the response of intra-cardiac hemodynamics to exercise test in patients with ischemic heart disease with similar lesions of the coronary arteries (patient selection for the aortocoronary bypass)]. 175 Oct 54

The effects of the Hemopump (HP) on left ventricular (LV) and coronary hemodynamics, with and without myocardial ischemia, were studied in an acute, anesthetized, open-chest dog preparation (n = 6). Coronary blood flow velocity in the left circumflex was assessed with an intracoronary Doppler catheter. Measurements were made at two pump speeds (minimal = HP1 and maximal = HP7) before coronary ligation (control), after ligation of the LAD (ischemia), and after induction of cardiac failure by multiple ligations of the diagonal branches (failure). Changing from HP1 to HP7 resulted in 1) Increased total cardiac output in ischemia and failure; 2) Increased mean aortic pressure and systemic vascular resistance in control, ischemia, and failure; 3) Decreased LV external work (LV systolic pressure X stroke volume) in control, ischemia, and failure; 4) Decreased LV end diastolic pressure in ischemia; 5) Decreased LV systolic pressure and pressure-rate product in failure; and 6) Increased coronary blood flow/O2 demand ratio in failure. Hemopump support reduced O2 demand by LV decompression, and improved blood flow/O2 demand ratio in the nonoccluded coronaries of ischemic, failing hearts.
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PMID:Effects of Hemopump support on left ventricular unloading and coronary blood flow. 175 Nov 87

Thirty-one patients, mean age 54 years, had been on chronic ambulatory peritoneal dialysis (CAPD) for an average of 38 months. Mean values (mg/dl) for triglycerides (567), total-C (267), LDL-C (133), and Apo-B (154) were elevated, and HDL-C (30) were low. The low values for total-C/Apo-B and LDL-C/Apo-B suggest an increase in the number of low density lipoprotein (LDL) particles, rather than in the amount of cholesterol per LDL particle. Without knowledge of lipids, ischemic heart disease for the 31 patients was categorized into five grades in the following manner. All patients were graded based on history (angina, myocardial infarction, and bypass surgery), electrocardiogram (EKG), and echocardiography. In addition, five patients underwent coronary angiography, the results of which were considered in their grading. The five grades were assigned as follows: Grade I, no evidence (n = 15); Grade II, angina with EKG ischemia (n = 4); Grade III, myocardial infarction (MI) (n = 1); Grade IV, MI with dyskinesia-akinesia on echo (n = 4); Grade V, severe three vessel disease on angiography, or multiple infarcts, or Grade IV with heart failure (n = 7). Only Apo-B (r = 0.56) and total-C/HDL-C (r = 0.57) correlated with severity of grade, with p less than 0.001. When patients with and without detectable ischemic heart disease were compared by stepwise logistic regression, Apo-B was the only variable that independently predicted heart disease (p = 0.001). However, contribution of the lipid changes induced by CAPD has not been established.
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PMID:Ischemic heart disease, serum cholesterol, and apolipoproteins in CAPD. 175 Dec 58


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