Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Carotid sinus hypersensitivity (CSH) is recognised in up to 45% of elderly patients with syncope, falls, and dizziness that may not be attributed to specific myocardial sinus node dysfunction, various diseases that affect pacemaker activity, cardiac output and blood supply to the brain. The pathophysiology of CSH is unclear but it is associated with ageing, hypertension, and ischaemic heart disease. CSH is potentially treatable with dual chamber pacing for prolonged sinus arrest (cardio-inhibitory CSH) but therapy for the more prevalent hypotension (vasodepressor CSH) is unsatisfactory. However, hypersensitivity of the carotid sinus is not consistent with the known blunting effects of senescence and hypertension on baroreflex sensitivity. The present hypothesis proposes that CSH in elderly patients results from up-regulation of brainstem postsynaptic alpha-2 adrenoceptors. Reduced carotid sinus compliance in elderly arteriosclerotic hypertensive patients will reduce afferent impulse traffic in the baroreflex pathway. Such relative deafferentation may be expected to cause baroreflex postsynaptic hypersensitivity, mediated by up-regulation of the dominant postsynaptic receptor population in the baroreflex pathway, ie, alpha-2 adrenoceptors. Vigorous carotid sinus stimulation, eg, massage, could thus cause an overshoot baroreflex efferent response, resulting in profound hypotension and bradycardia. Hypotension and bradycardia are compounded by the effects of age, hypertension, ischaemic heart disease and arteriosclerosis on rapid cardiovascular compensation, resulting in cerebral hypoperfusion and syncope. Thus CSH in elderly patients should be considered as a clinical marker of widespread arteriosclerotic disease, rather than as a distinct disease entity. If correct, this hypothesis has potentially important implications for the pharmacotherapy of hypotension-related symptoms in elderly arteriosclerotic patients.
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PMID:Pathophysiology of carotid sinus hypersensitivity in elderly patients. 756 34

Patients with hypertrophic cardiomyopathy are at increased risk for sudden death. Recent studies have improved our ability to risk-stratify such patients and have elucidated several potential mechanisms of sudden death and syncope. Certain noninvasive tests, such as signal-averaged electrocardiography and measurements of cardiac autonomic function and QT/QT dispersion, are often abnormal in hypertrophic cardiomyopathy, but are not useful for risk stratification. Myocardial ischemia determined by exercise thallium scintigraphy, however, identifies young patients with hypertrophic cardiomyopathy who are at high risk for cardiac arrest and syncope. Nonsustained ventricular tachycardia on ambulatory Holter monitoring in the absence of symptoms of impaired consciousness is associated with a benign prognosis and is not predictive of sudden death. Conversely, ventricular tachycardia induced at electrophysiologic study identifies adult patients with hypertrophic cardiomyopathy who subsequently experience sudden death. Finally, characterization of the natural history of the genetic defects will increasingly become an integral part of risk evaluation in hypertrophic cardiomyopathy.
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PMID:Identification of patients with hypertrophic cardiomyopathy at high risk for sudden death. 778 70

Hypertrophic cardiomyopathy (HCM) is the most common cause of death in the young, particularly in young competitive athletes. Death often occurs suddenly in asymptomatic, apparently healthy individuals. Several clinical parameters as well as genetic factors have been characterized that can identify those HCM patients who are at high risk for sudden cardiac death (SCD). The clinical parameters that have some predictive values for SCD in HCM patients are the following: a prior history of SCD, a family history of SCD, history of syncope, symptomatic ventricular tachycardia on Holter monitoring, inducible ventricular tachycardia during electrophysiologic studies, and myocardial ischemia in children with HCM. Recent identification of mutations in the beta myosin heavy chain gene and genotype-phenotype correlation in HCM patients have shown that the beta myosin heavy chain mutations are also prognosticators in HCM families. Several mutations such as Arg403Gln and Arg719Gln are associated with a high incidence of SCD, while Leu908Val mutation is associated with a benign course and a low incidence of SCD in HCM families. Additional genetic factors such as a polymorphism in angiotensin-converting enzyme I gene may also contribute to a high incidence of SCD in HCM families. Identification and characterization of HCM patients at high risk for SCD provide the opportunity to render prophylactic therapeutic interventions, such as implantation of defibrillators, in these individuals.
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PMID:Sudden cardiac death in patients with hypertrophic cardiomyopathy: from bench to bedside with an emphasis on genetic markers. 778 45

Unusual forms and causes of ischemic heart disease include angina pectoris in the presence of normal coronary arteries (syndrome X), congenital coronary abnormalities, vasculitic disorders, and graft atherosclerosis after cardiac transplantation. There is now evidence that endothelial dysfunction of coronary resistance vessels can account for abnormalities of the coronary microvasculature and possibly, myocardial ischemia and chest pain. The incidence of syndrome X appears to be higher in women, particularly those who have undergone hysterectomy. An intriguing hypothesis is that low estrogen levels may be associated with reduced expression of nitric oxide (reflecting endothelial dysfunction). The presence of coronary abnormalities in the young should not be underestimated. Syncope and arrhythmias are observed frequently in this patient population and warrant vigorous exploration. Worldwide, cardiac transplantation is now carried out in approximately 4500 patients yearly, with excellent (80% to 90%) 1-year survival due to improved immunosuppression. However, accelerated atherosclerosis develops rapidly postoperatively and is the main cause of late death. The link between cellular rejection of the myocardium and transplant coronary artery disease is not clear. The process of transplant coronary artery disease is believed to be due to chronic immune injury followed by intimal smooth-muscle proliferation and lipid deposition in the vascular wall. By the time it is detected by coronary angiography, the disease is far advanced and not susceptible to routine revascularization procedures. A prospective, randomized study of diltiazem versus no calcium blocker started early after transplantation has documented highly significant reductions in transplant atherosclerosis as measured by lumen narrowing, clinical events, and rates of retransplantation or death due to the process.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Unusual forms of ischemic heart disease. 791 90

A total of 38 patients with syncope in whom a cause was not assigned or suggested by the initial history, physical examination and electrocardiography (ECG) were studied. Twenty-four patients underwent cardiac examination with Holter ECG, electrophysiologic testing with programmed ventricular stimulation (EPS) and/or coronary arteriography including ergonovine provocation (ergonovine CAG). The study with Holter ECG, EPS and ergonovine CAG yielded a presumptive diagnosis in 36 patients (36/38 = 95%), 11 with vasopastic angina, 7 with ventricular tachycardia, 4 with ischemic heart disease, 9 with sick sinus syndrome (SSS), 1 with drug induced SSS, 3 with A-V block, 1 with supraventricular tachycardia, 1 with hypertrophic cardiomyopathy, 1 with aortic valve stenosis and 1 with carotid sinus syndrome (included are 1 patient with ventricular tachycardia+ischemic heart disease, 1 with SSS+vasopastic angina and 1 with ventricular tachycardia+vasospastic angina). Therapy based on these findings provided complete symptomatic relief in all patients during a mean follow up of 25 +/- 10 months (range 5-45 months). In conclusion, EPS and ergonovine CAG are useful in the diagnosis and therapy of unexplained syncope.
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PMID:Electrophysiologic study and ergonovine provocation of coronary spasm in unexplained syncope. 831 14

Arrhythmogenic right ventricular disease (ARVD) is a disease of unknown origin that primarily affects the right ventricle and is characterized by ventricular tachyarrhythmias which may lead to syncope and even, though rarely, sudden cardiac death. In 25 patients with ARVD, sympathetic innervation of the left ventricle was assessed by iodine-123 metaiodobenzylguanidine single photon emission tomography (123I-MIBG SPET). In addition, thallium-201 SPET was performed. The diagnosis of ARVD was made by an electrophysiological study and right and left heart catheterization including right ventricular endomyocardial biopsy. Ischaemic heart disease was excluded by coronary angiography. A group of seven patients without any evidence of heart disease served as a control group. Twenty-two of the 25 patients showed reduced uptake of 123I-MIBG. The abnormal areas were located predominantly in posterior and posteroseptal segments of the heart. No focus of increased 123I-MIBG activity could be demonstrated. No patient had signs of left ventricular involvement on left ventricular angiography. In contrast to the results of the 123I-MIBG SPET, those of 201T1 SPET were normal in 16 patients. The remaining nine patients showed areas of slight hypoperfusion not correlated with the reduced 123I-MIBG uptake. 123I-MIBG scintigraphy allows detection of left ventricular adrenergic dysinnervation in ARVD patients without morphological or functional abnormalities of the left ventricle.
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PMID:Sympathetic innervation of the left ventricle is impaired in arrhythmogenic right ventricular disease. 846 8

The authors describe a rare case of pulmonary thromboembolism with unusual clinical findings and emphasized the large difficulty encountered in formuling a correct diagnosis in a reasonable time. A man, 60 years old, was admitted to a Medical Division of our hospital for the appearance of chest pain and epigastric pain during effort in the last year. He smoked 20 cigarettes a day and drank wine (1 or 2 litres a day). He was affected by hypercholesterolemia and in the past reported relapsed thrombophlebitis in the left leg. Four years before admission to our hospital he underwent large and small left saphenectomy. He had no cardiac events in the past. After a non significant exercise stress test the patient was treated with nitrates and asa and was discharged from the hospital. At home the symptoms increased and after 8 months the patient was admitted again to the Cardiologic Division of the hospital. At admission he reported dyspnea and chest pain at rest, not only during effort and the ECG showed negative T waves in anterior and inferior leads. Intravenous heparine, nitrates and calcium antagonists stabilized the clinical picture. The following examinations revealed: reduction of the T wave negativity at the ECG registered during chest pain; mild enlargement of the heart at the chest roentgenogram; normal value of the left ventricle and apical and midseptal by ipokinesia at the transthoracic echocardiogram; normal coronary artery at the coronary arteriography. "Vasospastic angina" was diagnosed and the patient was discharged after 20 days, asymptomatic. After 15 days he returned to the hospital again for chest pain, dyspnea, hypotension and syncope despite therapy. At physical examination he showed a painful left tibio-tarsal tumefaction, an increased and splitting second heart sound in the pulmonary area and a systolic murmur in the third and fourth left interspace. The ECG showed a severe anterior ischemia, while a new transthoracic echocardiogram revealed a considerable dilatation of the right atrium, right ventricle and the main pulmonary artery with severe tricuspid regurgitation and pulmonary hypertension (mean PAP about 50 mmHg). The following pulmonary perfusion scintigraphy confirmed the diagnosis of pulmonary embolism and the selective right and left pulmonary arteriography exhibited multiple thrombi and large intravascular filling defects. The right heart catheterization confirmed a chronic precapillary pulmonary hypertension (mean PAP = 55 mmHg). About 24 hours after these examinations the patient died because of a cardiac arrest with electromechanical dissociation. Pulmonary thromboembolism is a potentially fatal disease characterized by a largely variable clinical presentation. Frequently pulmonary embolism diagnosis is difficult especially when clinical findings are unusual. In the case observed the "typical" chest and epigastric pains associated with the electrocardiographic findings directed diagnosis towards myocardial ischemia. Also after the coronary arteriography that showed normal coronary artery, the erroneous diagnosis persisted. Pulmonary embolism was correctly diagnosed too late to begin an effective therapy. These unusual clinical findings and diagnostic mistakes are stressed and critically reviewed in the article.
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PMID:[Pulmonary thromboembolism. A clinical case with unusual presentation]. 871 Jan 39

The authors analysed survival of 160 patients (121 men and 31 women; average age 57.2 +/- 12.5 years; follow-up 29 +/- 20 months) treated for malignant ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation, syncope with inducible ventricular tachycardia). The therapeutic evaluation was frequently invasive (145 patients underwent at least programmed ventricular stimulation, 108 patients underwent full endocavitary electrophysiological studies) and non-pharmacological therapy was widely used (defibrillator n = 44; antiarrhythmic surgery n = 28; ablative procedures n = 19; transplantation n = 7). The following underlying pathologies were observed: ischaemic heart disease n = 120; non-ischaemic left heart disease n = 19; right heart cardiac disease n = 4; and apparently normal hearts n = 17). The average ejection fraction was 40.5 +/- 15.5% and 29 patients were in the NYHA functional classes III or IV. Fifty-five patients had life-threatening arrhythmias whilst receiving amiodarone. At 2 years, the actuarial sudden death rate was 5.9 +/- 2.1% and the actuarial total cardiac mortality rate was 13.1 +/- 2.9%. Univariate analysis showed age, the presence of underlying cardiac disease, the presence of dilated cardiomyopathy, the absence of an invasive approach, the need for basal pacing in electrical cardioversion, the absence of betablocker therapy, a decreased left ventricular ejection fraction and a high NYHA functional class, to be predictive of sudden death. In multivariate analysis, age, the NYHA class for total cardiac mortality and the NYHA class for sudden death, were the only independent predictive factors. The authors conclude that in the era of invasive methods of evaluation and widespread use of non-pharmacological therapeutic methods, the symptomatology of cardiac failure assessed by the NYHA classification remains the most powerful independent prognostic factor after an episode of malignant ventricular arrhythmia.
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PMID:[Prognostic factors after sustained ventricular fibrillation or tachycardia. A multivariate study apropos of 160 cases]. 876 3

Syncope caused by cardiac asystole during dobutamine stress echocardiography occurred in a 60 year old woman presenting with chest pain and a non-diagnostic exercise test. Cardiac asystole was not associated with myocardial ischemia and was attributed to a powerful cardioinhibitory vagal reflex elicited by the stimulation by the drug of cardiac and aortic mechanoreceptors. Cardiac asystole was promptly reversed by the administration of atropine with no significant sequelae.
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PMID:Syncope caused by cardiac asystole during dobutamine stress echocardiography. 880 Oct 1

Although most of arrhythmia are secondary to cardiac disease, for example, ischemic heart disease and valvular heart disease, some types of arrhythmia are hereditary. Long QT syndrome (LQTS) is a hereditary cardiac disorder that causes syncope and sudden death from ventricular tachyarrhythmia. A boy eight years old, who had the familial history of LQTS in his sister and mother, admitted in our hospital. He had some episodes of syncope and markedly prolonged QT interval of 0.58 seconds in electrocardiogram. After follow-up of 12 years, he died suddenly because of interrupted medication including beta-blocker. Another patient with ventricular tachyarrhythmia also admitted. His family tree in which three young men died suddenly, revealed hereditary cardiomyopathy. Hereditary cardiac arrhythmia as shown the above clinically important because of prevention from sudden death, especially in young patients.
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PMID:[Hereditary cardiac arrhythmia]. 881 Aug


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