Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since 1977, six patients (five males and one female), aged 14 to 35 years, resuscitated from ventricular fibrillation, were referred to our department for detailed evaluation, after exclusion of major cardiac pathologic conditions. Four patients had a family history of heart disease. Basic ECGs showed sinus rhythm in all of them. PR interval was prolonged in one. Two patients had complete and one had incomplete right bundle branch block. One patient had inverted t waves in V1-3 and late potentials. Three had an upsloping ST-T segment elevation in V1-2. The cardiothoracic index was less than 0.5 in five and 0.50 in one. In one of the five patients studied, the clinical episode of ventricular fibrillation was reproduced by stimulation of the right ventricular outflow tract during electrophysiologic study. Results of cross-sectional echocardiography and angiography showed predominantly structural and wall motion abnormalities of the right ventricle in five patients and slight wall motion abnormalities of the left ventricle in two. Two patients also had mitral and tricuspid valve prolapse. Coronary arteries were normal in all five patients examined. Results of endomyocardial biopsy showed no abnormalities in one patient, fibrosis in two, and fibrolipomatosis in one. Two patients died during follow-up: autopsy was performed in one and results showed right ventricular cardiomyopathy. Thus in five of these selected patients with apparent idiopathic ventricular fibrillation, some abnormalities, predominantly of the right ventricle, were documented only after detailed investigation; however, clinical history and some nonspecific ECG abnormalities were factors in the diagnostic procedure.
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PMID:Ventricular fibrillation without apparent heart disease: description of six cases. 258 61

To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.
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PMID:[Early diagnosis and management of acute pulmonary embolism: clinical evaluation those of 225 cases]. 835 37

We report a patient with Brugada syndrome who developed sustained monomorphic ventricular tachycardia (SMVT). The patient was a 29-year-old man who experienced recurrent episodes of palpitation and syncope after drinking alcohol. Electrocardiogram showed right bundle branch block and ST-segment elevation in precordial leads V1-3 without Q-Tc prolongation. Organic heart disease and coronary artery disease were excluded by noninvasive and invasive tests. Ventricular fibrillation was induced by the application of a single extra-stimulus to the right ventricular outflow tract. During isoproterenol infusion, SMVT of left bundle branch block morphology (240/min) was induced by the application of a single extrastimulus to the right ventricular apex. SMVT also developed spontaneously. Pace mapping disclosed that SMVT originated at the free wall of the right ventricular outflow tract. Head-up tilt test and an alcohol provocation test both induced similar SMVT that was associated with hypotension and near syncope. SMVT was not terminated by intravenous administration of lidocaine, procainamide or adenosine triphosphate (10 mg), but was terminated by propranolol. Thus, a beta-adrenoceptor-mediated mechanism appears to play an important role in SMVT in this patient. The site of origin of SMVT might be closely related to the lesion that causes ST-segment elevation.
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PMID:Sustained monomorphic ventricular tachycardia in a patient with Brugada syndrome. 884 3

Brugada syndrome is characterized by ST-segment elevation in the leads V1-3 of electrocardiography (ECG) in the absence of a structural heart disease. A 26-year old male patient was admitted with sudden cardiac arrest. Cardiopulmonary resuscitation was successful and he was referred to the reanimation unit due to unconsciousness. A year before, he was diagnosed as having Brugada syndrome with type 1 ECG pattern at another center, at which time electrophysiologic study (EPS) was not performed due to lack of symptoms and a family history of sudden cardiac death. In addition, family screening revealed two asymptomatic brothers having Brugada syndrome with type 1 ECG pattern. Medical follow-up was recommended to one of them. The other sibling underwent EPS at a different center where ventricular fibrillation was induced. An implantable cardioverter defibrillator (ICD) was recommended, but the patient refused. A further analysis of the family made at our center showed type 2 ECG changes in the father and in one of the cousins. Due to the development of persistent brain injury and an expected survival of less than a year, an ICD was not considered in the patient. The prognostic value of EPS is still controversial in asymptomatic patients with type 1 Brugada syndrome, without a family history of sudden cardiac death.
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PMID:[A case of asymptomatic Brugada syndrome with type 1 ECG pattern and cardiac arrest: an evaluation of the prognostic value of electrophysiologic study]. 2067 99

Brugada syndrome is associated with sudden cardiac death in patients with a structurally normal heart. The electrocardiogram (ECG) pattern of Brugada syndrome is characterised by complete or incomplete right bundle branch block and ST-segment elevation in the right precordial leads. These ECG signs may not always be apparent but can be unmasked with certain anti-arrhythmia agents. We report here a case of a 26-year-old woman without detectable structural heart disease but with a history of syncope, cardiac arrest, intubation and defibrillation for ventricular fibrillation. We performed challenge tests with propafenone and ajmaline. After infusion of propafenone, there were minimal ECG changes which were not diagnostic for Brugada syndrome. One week later the provocation test was repeated with ajmaline. During infusion of ajmaline, prominent J waves and ST-segment elevation appeared in the right precordial leads (V1-3). Premature ventricular complexes were seen on a 12-lead ECG. The patient's ECG showed Brugada type 1 pattern. She received an internal cardioverter/defibrillator and was discharged with a beta-blocker.
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PMID:Is a drug-challenge test with propafenone adequate to exclude Brugada syndrome? 2361 2