Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study retrospectively assesses the underlying causes of sudden unexpected death and the occurrence of prodromal symptoms in 162 subjects (aged 9 to 39 years) over a 10-year period (1976 to 1985). Underlying cardiac diseases accounted for sudden death in 73% and noncardiac causes in 15% of subjects. In 12% of subjects, the causes were unidentifiable. Myocarditis (22%), hypertrophic cardiomyopathy (22%) and conduction system abnormalities (13%) were the major causes in 32 subjects aged less than 20 years. Major causes of 46 deaths in subjects 20 to 29 years were atherosclerotic coronary artery disease (24%), myocarditis (22%) and hypertrophic cardiomyopathy (13%). The largest number of deaths in 84 subjects aged greater than or equal to 30 years was attributed to coronary artery disease (58%), followed by myocarditis (11%). Among noncardiac causes of sudden death, intracranial hemorrhage was the most frequent (5%), followed by infectious disease (4%). Prodromal symptoms were reported by 54% of subjects; most frequent were chest pain (25%) in subjects aged greater than or equal to 20 years, and dizziness (16%) in those aged less than 20. Sudden death, which occurred during routine daily activity in 49% and during sleep in 23% of subjects, was related to physical exercise in 23% and emotional upset in 6%. Sudden unexpected death in the young is still an unresolved medical problem. The early recognition of prodromal symptoms could be crucial in the prevention of sudden death, specifically when exercise-related.
 ...
PMID:Sudden unexpected death in persons less than 40 years of age. 195 Nov 30

Forty-four cases of hypertrophic cardiomyopathy (23 men, 21 women; 55 +/- 15 years) referred for evaluation of chest pain (28 cases), dyspnoea (26 cases), palpitations (25 cases), dizziness (11 cases) and syncope (4 cases), were investigated prospectively between February 1983 and February 1989. The cardiomyopathy was concentric (N = 16), obstructive (N = 24) or apical (N = 4) and the diagnosis confirmed by angiography. Twenty-four hour Holter monitoring showed no ventricular extrasystoles in 43% of patients: the others had Grade I (25%), Grade III (2%), Grade 4A (14%) or 4B (16%) ventricular arrhythmias with diurnal predominance in half the cases. Patients with greater than or equal to Grade III ventricular extrasystoles had greater left axis deviation but did not differ from the others from the hemodynamic point of view. Exercise stress testing induced an isolated ventricular arrhythmia in 23% of patients and repetitive extrasystoles in 23%. The prevalence of surface late ventricular potentials was no greater in these patients than in normal subjects (4% vs 1%; NS). Programmed ventricular stimulation (N = 37) induced a repetitive response in only 25% of patients, with only two cases of sustained monomorphic ventricular tachycardia. There were no correlations between the results of programmed ventricular stimulation and those of Holter monitoring, exercise stress testing or late ventricular potential recording, but patients with inducible ventricular tachycardia or fibrillation had proportionally more syncopal episodes and greater than or equal to Grade III ventricular extrasystoles on Holter monitoring, but the difference was not statistically significant in this series.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Study of the arrhythmogenicity of cardiomyopathies. Hypertrophic cardiomyopathies]. 204 23

In order to develop the tentative criteria of the differential diagnosis, 18 patients with obstructive hypertrophic cardiomyopathy (OHCMP), 3 with nonobstructive hypertrophic cardiomyopathy (NOHCMP), 8 with essential hypertension (EH) with inadequate left ventricular hypertrophy (LVH) and 10 normal persons were subjected to clinical examination and to ultracardiosonography. The patients with OHCMP mainly complained of dizziness and syncopes. Since childhood they had systolic murmur and ECG abnormalities. Ultracardiosonography showed asymmetrical LVH, a considerable decrease of the ventricular cavity as well as abnormalities of the localization and function of the papillary muscles. NOHCMP was marked by the combination of the good well-being of the patients with gross abnormalities on the ECG. Ultracardiosonography demonstrated moderately pronounced and asymmetrical LVH. The group suffering from EH with inadequate LVH was characterized by the early development of severe circulatory failure with arterial hypertension of moderate intensity. The changes in the architectonics of the left ventricle and its subvalvular structures turned out to be similar to those in OHCMP but were less remarkable.
 ...
PMID:[The differential diagnosis of various forms of hypertrophic cardiomyopathy and hypertension with inadequate left ventricular hypertrophy]. 253 35

Hypertrophic cardiomyopathy (HCM) is a primary myocardial disease of unknown cause that is characterized by a hypertrophied, nondilated, hypercontractile left ventricle. Its etiology and pathogenesis remain undefined but the three principal factors implicated are a genetic predisposition, a hypersensitivity to catecholamines, and an abnormal calcium metabolism. The hypertrophy typically involves the intraventricular septum to varying degrees, but may also involve the apex or free wall and even be concentric. The disease occurs in either an obstructive or a nonobstructive form depending on whether an intraventricular pressure gradient can be demonstrated at rest or on provocation. The gradient and obstruction to outflow is usually seen in patients with asymmetric septal hypertrophy (ASH) and anterior motion of the mitral valve during systole (SAM). Abnormal left ventricular diastolic function characterized by inadequate filling and impaired relaxation has been shown to be very important in both the obstructive and nonobstructive forms of the disease. In addition, inadequate coronary vasodilator reserve as a result of small vessel disease, microvascular spasm, and/or low capillary density per unit myocardial mass has been implicated as an important cause of ischemia in patients without coronary artery disease. HCM is a disease of young adulthood with relatively slow progression; young patients are often asymptomatic, whereas older patients are more limited by dyspnea, angina, dizziness, or syncope. Supraventricular tachyarrhythmias occur in 30% of patients, and high-grade ventricular arrhythmias occur in over 75%. The annual mortality is 3-5%. The common mode of demise is sudden cardiac death. Therefore, the primary objectives of treatment are the amelioration of symptoms, the control of arrhythmias, and the prevention of sudden death. Beta-adrenoreceptor blocking agents decrease myocardial contractility and oxygen demands and increase ventricular volume; therefore, they are most useful in patients with the obstructive form of HCM. Calcium channel antagonists enhance left ventricular relaxation, relieve microvascular spasm, and improve coronary filling and therefore are the agents of choice in patients with diastolic dysfunction. The ability of the calcium channel antagonists to decrease contractility makes them valuable in patients with obstructive HCM. Arterial vasodilators, diuretics, nitrates, and inotropic agents should be avoided because they can increase the intraventricular gradient. Myomyectomy is reserved for those patients with the obstructive form of HCM whose symptoms are refractory to medical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37

A prospective study of arrhythmias was performed in 33 patients with hypertrophic cardiomyopathy with obstruction by Holter monitoring. The aim of the study was to assess the incidence of "occult" arrhythmias in this condition and to establish a "profile" of high risk patients from clinical, echocardiographic and haemodynamic data. The Holter monitoring demonstrated asymptomatic arrhythmias in 31 of the 33 patients (94%). A supraventricular arrhythmia was detected in 15 cases (45%), including 7 episodes of supraventricular tachycardia (21%). Ventricular arrhythmias were observed in 28 patients (85%), including 5 episodes of ventricular tachycardia (15%). Some patients presented several types of arrhythmia. A number of patients with arrhythmia including short bursts of ventricular tachycardia were asymptomatic during Holter monitoring; conversely, other patients complained of dizziness or syncope but had no arrhythmias. A retrospective study of clinical, echocardiographic and haemodynamic data showed no difference between patients with and patients without arrhythmias. Medium-dose betablocker therapy (propranolol, 110 mg/day) did not seem to protect patients with hypertrophic cardiomyopathy with obstruction from arrhythmias. We conclude that Holter monitoring should form part of the routine evaluation of patients with cardiomyopathy with obstruction, and that potentially dangerous arrhythmias should be treated by anti-arrhythmic agents other than betablockers. This attitude could reduce the incidence of syncope and eventually decrease the risk of sudden death in this condition.
 ...
PMID:[Long-duration electrocardiographic recording in 33 patients with obstructive cardiomyopathy]. 643 35

There were 84 confirmed cases of congestive (or dilated) cardiomyopathy (CCM or DCM), 57 of hypertrophic nonobstructive cardiomyopathy (HNCM) and 52 of hypertrophic obstructive cardiomyopathy (HOCM) collected from 15 cardiology divisions of university or national hospitals in Japan. Out of the 193 patients with cardiomyopathy, 145 (75%) were male and 48 (25%) female (M/F ratio = 3:1). The mean age of the patients was 34.1 years. Patients with HNCM or HOCM were usually asymptomatic, but palpitation was the most common symptom, followed in frequency by chest oppression, dyspnoea, chest pain, arrhythmia and syncope in HNCM, and by dyspnoea, chest oppression, chest pain, dizziness and syncope in HOCM. ST-T abnormalities were most frequently observed, 90.3% in HNCM and 86.3% in HOCM. Left ventricular hypertrophy was observed in 76.4% of HNCM and in 79.1% of HOCM. Abnormal Q waves were observed equally in HNCM (32.4%) and in HOCM (35.3%). A fourth sound was more common (69.2% in HNCM; 75.8% in HOCM) than a third sound (39.7% in HNCM; 36.5 in HOCM). The heart size on conventional radiography was within normal limits or slightly enlarged; the mean cardiothoracic ratio was 0.52 in HNCM and 0.54 in HOCM. A cumulative survival rate in 149 patients with hypertrophic cardiomyopathy demonstrated that the 10-year survival rate after the time when the diagnosis was made was 34.2% for CCM, 81.7% for HNCM and 84.4% for HOCM. Autopsy studies in 11 patients with hypertrophic cardiomyopathy revealed that marked fibre disarray of the heart could be detected by the endomyocardial biopsy of the right ventricular septum in 40% at most of the patients with hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypertrophic obstructive and non-obstructive cardiomyopathy in Japan. Diagnosis of the disease with special reference to endomyocardial catheter biopsy. 668 27

An evaluation was undertaken regarding two female patients suffering from obstructive hypertrophic cardiomyopathy, with high and strongly symptomatic gradients, as well as evidencing a resistance to medication with beta-blockers, verapamil and disopyramide when administered in maximal doses. These patients were provided with the implant of a definitive type DDD pacemaker, with an auricular electrocatheter placed on the right auricular appendix, and with a bipolar ventricular catheter placed on the apex of the right ventricle. The generator was programmed with a short AV so as to ensure that the ventricular stimulation would at any given time be the result of the ventricular contraction would be initiated at the apex portion of the right ventricle. With these therapeutics, we observed not only a reduction or even the gradient, but also the complete elimination of the existing symptoms--angor, dyspnea, dizziness, palpitations and fainting--with the resulting normalcy of the quality of life of the patients. All taken into account we are of the opinion that these therapeutics are, in the case of patients suffering from obstructive hypertrophic cardiomyopathy, a valid alternative for surgical treatment by means of myectomy or myotomy, but without the morbidity and mortality rates presented by such methods.
 ...
PMID:[Acute and chronic sequential atrioventricular pacing in patients with obstructive-type hypertrophic myocardiopathy resistant to medical therapy]. 757 64

Hemodynamic syncope is caused by an impediment to a necessary increase of the cardiac output; therefore, hemodynamic syncopes most often occur during or shortly after exercise. However, a syncope at rest does not exclude a hemodynamic cause. Moreover, arrhythmias which may directly lead to syncope or accentuate the hemodynamic impediment are often present in cardiac diseases causing hemodynamic syncope. Hemodynamic syncopes are responsible for 2 to 3% of all syncopes leading to medical evaluation. Of these, more than half are caused by aortic stenosis and about one quarter by pulmonary embolism. Other reasons are rare. Hypertrophic cardiomyopathy is more often associated with arrhythmic than with hemodynamic syncope. Syncope in primary pulmonary hypertension is often preceded by dizziness, epigastric distress and faintness. Since the medical therapy may lead to hemodynamic deterioration, it must be started under invasive observation. Primary tumors of the heart are rare; secondary cardiac neoplasms are 6 to 40 times more common. Myxoma is the most common primary tumor of the heart. It is important to promptly undertake surgery in order to improve prognosis. Various other diseases may provoke hemodynamic syncope; however, other symptoms are by far more common.
 ...
PMID:[Hemodynamically-induced syncope]. 933 77

Mutations of the cardiac beta-myosin heavy-chain (beta-MHC) gene cause hypertrophic cardiomyopathy (HCM). Recent genotype-phenotype correlation studies have shown that mutations carry prognostic significance. We studied five unrelated Chinese families with hypertrophic cardiomyopathy. Exons 3-27 and 40 of the beta-MHC gene were screened with both the polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) method and the cycle sequencing of the PCR products. A previously reported heterozygous mutation Arg719Gln (arginine-->glutamine in codon 719) in exon 19 was found in one family. The proband is a 30-year-old female diagnosed at age of 25 years when she presented with symptoms of chest pain, palpitations, and frequent incidents of dizziness and syncope. A two-dimensional echocardiogram showed moderate asymmetrical septal hypertrophy with left atrial enlargement. There was no obstruction of the left ventricular outflow tract (LVOT). The patient also developed atrial fibrillation. The proband's mother and one of her sisters had similar clinical manifestations and both died suddenly at the age of 38 years. In addition, two silent nucleotide substitutions (ACT63ACC, TTT244TTC) in the cardiac beta-MHC gene were identified in the other four families. These synonymous mutations did not cosegregate with the disease in the families and they were also present in the 60 healthy and age-matched control subjects. Of the five families studied, we did not find any missense mutation in the remaining four families. The missense mutation Arg719Gln found in the Chinese family is associated with a malignant phenotype of severe clinical symptoms and poor survival prognosis. This mutation also causes atrial enlargement and atrial fibrillation. Our study provides further evidence that the mutation, which alters the charge of the myosin heavy chain, is associated with a serious clinical outcome.
 ...
PMID:A malignant phenotype of hypertrophic cardiomyopathy caused by Arg719Gln cardiac beta-myosin heavy-chain mutation in a Chinese family. 1149 78

A 71-year-old woman had hypertrophic cardiomyopathy associated with midventricular obstruction and an apical aneurysm in the left ventricle. She had had abnormal electrocardiograms for more than 30 years and for the past year had been suffering from occasional attacks of dizziness and low systemic blood pressure. Holter 24-h electrocardiographic monitoring revealed ventricular paroxysmal contractions (676/day) with nonsustained ventricular tachycardia. Doppler echocardiography revealed paradoxical jet flow from the apical aneurysm to the left ventricular outflow during early diastole. Magnetic resonance imaging depicted midventricular hypertrophy and a dyskinetic thin apical wall, which were confirmed by angiography. Coronary angiograms showed no narrowing of the major extramural coronary arteries, but there was compression of aberrant coronary arteries apparently feeding the hypertrophic portion of the left ventricular wall. Stress thallium-201 myocardial imaging showed a persistent severe defect in the left ventricular apex. A hemodynamic study revealed low cardiac output and an intraventricular pressure gradient (approximately 90 mmHg) between the left ventricular apical high-pressure chamber and the subaortic low-pressure chamber. The present case represents a rare combination of hypertrophic cardiomyopathy, midventricular obstruction, and an apical aneurysm in an elderly woman. Myocardial ischemia may have played an important role in the genesis of the apical aneurysm.
 ...
PMID:Hypertrophic cardiomyopathy with midventricular obstruction and apical aneurysm: a case report. 1166 99


1 2 Next >>