UMLS:C0018801 - FACTA Search

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

The real incidence of pacemaker implants for carotid sinus syndrome (CSS) and the relation between CSS and sick sinus syndrome (SSS) is not precisely known. Patients who needed pacing therapy because of atrial bradyarrhythmias were investigated by means of carotid sinus massage, dynamic ECG, and invasive electrophysiological sinus node evaluation. Of 298 consecutive patients receiving a pacemaker implant, 36 (12%) had a severe cardioinhibitory carotid sinus reflex with reproducible spontaneous symptoms (CSS), 33 (11%) had sinus bradycardia less than 50 beats/min or an abnormal electrophysiological evaluation (SSS) and 24 (8%) had both (CSS + SSS). The annual incidence was 40, 37, and 26, respectively, implants per year/million of inhabitants (total incidence 325). Patients affected by CSS, if compared with those affected by SSS, showed: a higher prevalence of syncope (97% vs 42%); more syncopal episodes per patient (2.9 +/- 2 vs 1.8 +/- 0.9); a lower prevalence of associated cardiac diseases (53% vs 100%); cardiac enlargement (36% vs 88%); heart failure (6% vs 36%) and paroxysmal atrial fibrillation (0% vs 42%); and a more frequent indication for VVI pacing (75% vs 3%). In patients with CSS + SSS, intermediate characteristics were present. In conclusion, CSS is as frequent an indication to cardiac pacing as SSS; clinical differences justify a distinction between them, even if they are associated in 26% of cases.
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PMID:Pacing for carotid sinus syndrome and sick sinus syndrome. 170 95

The aim of this study was to evaluate retrospectively the outcome of 101 patients who were assigned to long-term therapy with propranolol (55 patients) or verapamil (46 patients) between 1980 and 1988. Baseline clinical, electrocardiographic, and echocardiographic data were similar in both groups. Exclusion criteria were the evidence of complex ventricular arrhythmias, a family history of the disease and/or sudden death, previous syncopal episodes, or left ventricular dysfunction. During a mean follow-up of 4 +/- 3 years (range: 1-9 years), side effects were more commonly recorded in patients who were treated with verapamil rather than in propranolol-treated patients (8 vs. 3, respectively), though the difference was not statistically significant. Sixteen patients (13 propranolol-treated patients and three verapamil-treated ones, p less than 0.05) died suddenly while on treatment. In addition, three patients who stopped verapamil because of adverse reactions died from heart failure after withdrawal, but before the end of the follow-up period. The assessment of total mortality on the intention-to-treat basis showed that death due to cardiac causes occurred in 13 propranolol-treated patients and in six verapamil-treated patients (ns). Thus, verapamil was more effective than propranolol in preventing sudden death during long-term therapy of "low-risk" patients with hypertrophic cardiomyopathy, though its administration was associated with the occurrence of non-sudden cardiac deaths and a high incidence of side effects.
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PMID:Hypertrophic cardiomyopathy: long-term effects of propranolol versus verapamil in preventing sudden death in "low-risk" patients. 208 Nov 44

A cardiac fibrosarcoma involving the right ventricular free wall, the interatrial septum, and proximal portion of the interventricular septum, with a 2-cm diameter protrusion into the right atrial lumen, was found at necropsy of a 2-year-old Miniature Schnauzer. Severe distortion of the tricuspid valve and narrowing of the aortic and pulmonic outflow tracts had caused the dog to develop right-sided cardiac failure and to have syncopal episodes. A tentative antemortem diagnosis of congenital pulmonic stenosis had been made on the basis of results of physical examination and diagnostic work-up. Evaluation of the case exemplifies the difficulty encountered in diagnosing cardiac tumors before the patient's death.
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PMID:Cardiac fibrosarcoma in a dog. 380 49

We report two cases of classic pacemaker syndrome. Both patients developed severe clinical manifestations after implantation of a VVI pacemaker. One patient presented syncopal episodes and the other one manifest cardiac heart failure. Additionally, we review the mechanisms responsible for this clinical entity.
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PMID:[Classical pacemaker syndrome. Report of 2 cases with severe clinical manifestations]. 876 16

Bernardo O'Higgins was a very apprehensive individual regarding his health and ailments. This fact is clearly reflected in his letters, that provide valuable anamnestic data. During his youth, while living is Spain, he suffered of yellow fever and later in Chile, he probably had an acute phase of a rheumatic fever. Since his adolescence, he was affected by a chronic hlepharo-conjunctivitis. During the Chilean independence revolution, he suffered several battle wounds. The most severe was a shot that affected both his right arm and elbow (1818). While living in Peru (1823-1842) he suffered of dysentery and malaria. The latter was an endemic disease in the valleys of Peru. Being previously asymptomatic, he started experiencing extensional dyspnea, angor pectoris and syncopal episodes in 1840. At that time, physicians diagnosed a hypertrophic cardiomyopathy. Analyzing his symptoms and taking into account their short term evolution, the author concludes that they were a consequence of either an aortic stenosis or coronary insufficiency. These led him to a heart failure that was his immediate cause of death in 1842.
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PMID:[A medical history of Bernardo O'Higgins (1778-1842)]. 1066 97

Patients with a history of myocardial infarction and complete bundle branch block with syncopal episodes have a high risk of sudden death: the identification of the cause of the syncope is therefore essential. The aim of the study was to assess the diagnostic value of non-invasive techniques used in the investigations of syncope: 24 hour Holter recording, high amplification ECG and measurement of left ventricular ejection fraction. The results of these investigations were compared with those of complete electrophysiological investigation evaluating atrioventricular conduction and the inducibility of tachycardia. The patient population was 134 patients, 83 with right bundle branch block and 51 with left bundle branch block. Ninety one patients had inducible sustained ventricular tachycardia and 24 had atrioventricular conduction defects: of these, 14 also had ventricular tachycardia. During follow-up, there were 12 sudden deaths and 13 deaths from cardiac failure. Uni- and multivariate analysis showed induction of ventricular tachycardia to be a significant risk factor for global mortality and sudden death but prolongation of the averaged QRS complex (> 165 msec) was also an independent risk factor of global cardiac mortality. The authors conclude that simple prolongation of the averaged QRS duration > 160 ms in patients with right bundle branch block and > 170 ms in patients with left bundle branch block after myocardial infarction and syncope is a significant poor prognostic factor. However, this sign is not predictive of sudden death.
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PMID:[Prolongation of the averaged QRS complex. A simple prognostic factor in patients with post-infarction bundle branch block and a history of syncope]. 1119 Apr 56

Syncope in patients with advanced heart failure is a sign of poor prognosis. The cause of syncope in patients with dilated cardiomyopathy (DC) is not fully recognized and may remain elusive even after standardized evaluation. The purpose of the present study was to examine the implication of neurally mediated mechanisms in the pathophysiology of syncopal episodes in patients with DC. Twenty-six patients (21 men, 5 women; mean age 59 +/- 2 years, range 38 to 79) with DC and left ventricular ejection fractions <or=40% were included in the study. Thirteen patients with unexplained syncope or presyncope and a control group of 13 patients without unexplained syncope underwent head-up tilt tests with clomipramine challenge. The 2 groups were matched with regard to age, gender, and left ventricular ejection fractions, and there were no major differences in terms of medication. Heart rate variability analysis and plethysmography of forearm flow were performed during the tilt tests. Blood samples were also drawn for catecholamine measurements. In the group with histories of unexplained syncope, the head-up tilt test results were positive in 11 patients (84.6%). Sympathetic and parasympathetic heart rate indexes were markedly stimulated, while catecholamine concentrations and blood flow changes indicated sympathetic withdrawal during tilting. In the control group, the head-up tilt test results were negative in 12 patients (92.3%). In conclusion, neurally mediated mechanisms seem to be implicated in the pathophysiology of syncope in patients with DC and should therefore be considered in the differential diagnosis of syncopal episodes of unexplained origin.
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PMID:Neurocardiogenic mechanisms of unexplained syncope in idiopathic dilated cardiomyopathy. 1729 3

History A 46-year-old woman was admitted to our hospital with decompensated congestive heart failure and pericardial effusion diagnosed on echocardiography. She had no family history of sudden cardiac death. She was born at term and experienced no cardiac events until 4 years of age, at which point she was hospitalized because of three syncopal episodes that were not related to exercise. Over the next 10 years, she experienced two additional episodes of syncope not related to exercise. She had another hospital admission at 12 years of age. Clinical examination did not reveal cyanosis or clubbing, peripheral pulses were normal, and blood pressure was 90/60 mmHg. Her venous pressure was elevated, but the liver was not enlarged, and the lung fields were clear. Electrocardiography showed sinus rhythm, right bundle branch block, T-wave inversion in V6, and evidence of right atrial dilatation. Two-dimensional echocardiography showed normal intracardiac connections, with the tricuspid valve in the normal position and normal size of the left atrium and left ventricle with a normal ejection fraction. The right ventricle was dilated without evidence of right ventricular outflow tract obstruction. Implantation of an implantable cardioverter-defibrillator was considered but was ultimately contraindicated because of right ventricle anatomy. Thus, the patient received conservative care and was started on digoxin and diuretics. At 32 years of age, she experienced an episode of atrial flutter that was treated with electrical cardioversion. As stated earlier, at 46 years of age, she was admitted to our hospital with decompensated heart failure to be evaluated for a heart transplant. She underwent electrocardiography, echocardiography, cardiac MRI with and without administration of contrast media, and non-cardiac-gated multidetector CT with and without contrast media to rule out pulmonary embolism. The following quantitative results were obtained with MRI: Left ventricular end-diastolic volume (LVDV) was 40 mL (LVDV per body surface area [BSA], 25 mL/m²); left ventricular end-systolic volume (LVSV), 21 mL (LVSV/BSA, 13 mL/m²); stroke volume (SV), 19 mL (SV/BSA, 12 mL/m²); and ejection fraction, 47%. Right ventricular end-diastolic volume (RVDV) was 262 mL (RVDV/BSA, 164 mL/m²); right ventricular end-systolic volume (RVSV), 198 mL (RVSV/BSA, 124 mL/m²); stroke volume (SV), 64 mL (SV/BSA, 40 mL/m²); and ejection fraction, 24%. Phase contrast sequences in the aorta and pulmonary artery showed systemic output of 20 mL and pulmonary output of 18 mL. Tricuspid regurgitation was massive (46 mL) (Figs 1-4).
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PMID:Case 288. 3319 73