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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

We have developed a new surgical method for repairing tracheobronchomalacia. In experiments on dogs we tried external fixation of Marlex mesh (Bard Cardiosurgery Division, Bellerica, Mass.) on the trachea. We first made models of tracheomalacia by making fractures or resections in intrathoracic tracheal cartilages and then made an external fixation of Marlex mesh on the malacic segments of the trachea. In 11 dogs Marlex mesh was sutured onto the trachea with absorbable thread. The trachea was firmly supported after 2 to 6 months, compared with three controls in which no external fixation was made. However, mucosal defects associated with ischemia caused by the suture developed in four of the 11. In 13 more dogs Marlex mesh was bonded to the trachea with fibrin glue. After 3 to 8 months the supporting strength of the trachea increased up to the level of the normal trachea. There was no evidence of inflammation or of mucosal defects. Therefore Marlex mesh was applied to a 44-year-old-man who had experienced frequent attacks of cough syncope. After the operation the attacks of cough syncope and collapsing of his airway disappeared completely.
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PMID:Development of a new surgical procedure for repairing tracheobronchomalacia. 221 35

A 64-year-old woman with a history of hypertension for ten years and of syncope 18 month previously visited our Division of Cardiology on 12 June, 1989. The S4 and mitral regurgitation were audible at the apex, and her electrocardiogram showed ST-depression in leads II, aVF, V5-6 and prominent U-wave (PU) in V1-3 when first seen. Then, she was thought to have a posterior myocardial ischemia. PU in V1-3 diminished whereas T-wave increased after nitrate and Ca++ blocker. Ergometer exercise ECG showed ST-depression in II, III, aVF, V4-6 and PU with decreased T-wave in V2-3 with no apparent symptoms. Simultaneously, Tl-201 myocardial imaging demonstrated a transient posterior defect. A silent posterior myocardial ischemia was, therefore, confirmed. Coronary arteriograms demonstrated subtotal obstruction of the proximal left circumflex artery, and the peripheral site was filled by collaterals from the right coronary artery. Angina-induced PU in the right precordial leads proved to be useful in detection of posterior myocardial ischemia, and this marker may also improve the possibility of detection of silent posterior ischemia.
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PMID:[A case of silent posterior myocardial ischemia/left circumflex artery obstruction detected by prominent U-wave in right precordial leads]. 228 23

We retrospectively analyzed the clinical data of 146 patients admitted to a general hospital with the diagnosis of syncope. A definite or highly likely cause was identified in 91 patients (62%). These were of cardiovascular origin in 78%: conduction defects (31), sinus node disease (9), obstructive causes (8), ventricular arrhythmia (8), ischemia (5) and miscellaneous (14). A non cardiovascular origin was present in 22% of patients: intoxication (7), hysteria (5), hypoxemia (3), vasovagal (2), gastrointestinal bleeding (2) and 2 others. The final diagnosis in patients with a known cause was established by the history and physical examination in 16, the ECG in 42, Holter 9, ECG monitoring in ICU 8 and echocardiogram 6. No difference in the distribution of causes was present between patients below or above 65 years of age. In hospital mortality was 2%.
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PMID:[Syncope: general characteristics and its relation to age]. 251 98

Three patients with an anomalous main coronary artery coursing between the great vessels are presented with a review of the literature. Their surgical treatment by coronary artery bypass grafting with use of the ipsilateral internal mammary artery is described with angiographic follow-up. Young patients with these anomalies, whether they are asymptomatic or have syncope, are at high risk for sudden death. Older patients with angina appear to be adequately risk stratified by thallium stress tests. For patients requiring surgical intervention, aortoplasty and coronary artery bypass grafting have both resulted in relief of symptoms, but the follow-up is limited. We suggest that coronary artery bypass grafting with an ipsilateral internal mammary artery graft to the anomalous vessel is the procedure most likely to relieve ischemia and achieve good long-term results for both symptomatic relief and survival.
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PMID:Surgical therapy in the management of coronary anomalies: emphasis on utility of internal mammary artery grafts. 265 51

A 31-year-old man with allergic rhinoconjunctivitis and asthma experienced an episode of anaphylaxis following an injection of allergens during hyposensitization. His anaphylactic episode was remarkable because of a relative sinus bradycardia at the beginning of his reaction. This case is reported to highlight the importance of not confusing the anaphylactic syndrome with vasovagal syncope even when a tachycardia is initially absent. The possible pathophysiologic role of right coronary vasospasm resulting in the Bezold-Jarish reflex or sinoatrial node ischemia is discussed.
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PMID:Anaphylaxis associated with relative bradycardia. 273 57

Loss of consciousness is rare in the absence of transient or persistent insult to the diencephalon or mesencephalon. We found three patients with severe atherosclerotic stenosis or occlusion of both internal carotid arteries who experienced brief loss of consciousness. Common characteristics were the absence of clinical or electroencephalographic seizure activities, significant cardiovascular disease, or a history suggestive of vasovagal syncope. Angiographically, the patients had widely patent vertebrobasilar circulation and collaterals from vertebrobasilar to carotid circulation. Episodic loss of consciousness disappeared after carotid endarterectomy. We concluded that bilateral hemispheric ischemia caused brief loss of consciousness, but selective focal ischemia in the subcortical structures superimposed on widespread bihemispheric ischemia may have been responsible. Since loss of consciousness is rare in carotid occlusive diseases, systemic and vertebrobasilar causes must be carefully ruled out in each instance.
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PMID:Brief loss of consciousness in bilateral carotid occlusive disease. 275 25

To return to the patient's syncopal episode, it is clearer now that he probably did have a vasovagal reaction. An hour had elapsed since administration of morphine, making that etiology unlikely. The patient showed no evidence of heart block or acute ischemia. While nitrate induced hypotension may have contributed to his faint, that would not have explained his bradycardia. Worth noting is the fact that he developed nausea and lost consciousness as an arterial puncture was about to be performed. Had he been asked, the patient might have recalled other incidents of vasovagal fainting. A combination of factors may cause a brief syncopal episode in the ICU. Sorting out the causes of vasovagal syncope may be difficult if not impossible, and a syncopal episode may set a chain of events into motion that further complicates the situation. The patient with an acute, especially inferior MI who received intravenous medications is particularly prone to vagal-like reactions. Patients with nausea or extreme anxiety should be watched carefully and their symptoms treated.
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PMID:Vasovagal syncope. 280 52

While programmed electrical stimulation of the heart is useful in directing therapy in cardiac arrest survivors who exhibit inducible ventricular tachycardia (VT), controversy exists as to the risk of recurrent ventricular fibrillation (VF) and need for antiarrhythmic therapy in patients without inducible VT during drug-free control programmed stimulation studies. In this study, the clinical features and arrhythmic outcome of 43 survivors of VF without inducible VT at control programmed stimulation were examined. In 38 patients, factors that may have played a potentiating role in the genesis of VF included ischemia in 15, proarrhythmia in 18, rapid rate response to atrial fibrillation in 3 and acute alcoholism in 2. Three patients required antiarrhythmic drugs for supraventricular tachyarrhythmia and 40 patients were discharged without antiarrhythmic therapy. At 32 +/- 21 months (range 1 to 82), 37 (92%) have remained free of arrhythmic recurrence while 3 have had sustained subsequent major arrhythmic events (syncope 1 patient, VF 1, sudden cardiac death 1). Thus, survivors of VF without inducible VT at drug-free control programmed stimulation are characterized by (1) potentiating factors--often identifiable and correctable--that may be important to the genesis of VF; (2) generally low risk of arrhythmic recurrence; and (3) effective long-term management often achieved without the use of additional antiarrhythmic drugs or antitachycardia/defibrillation devices.
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PMID:Long-term arrhythmic outcome in survivors of ventricular fibrillation with absence of inducible ventricular tachycardia. 319 83

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)
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PMID:Hypertrophic cardiomyopathy: current views on etiology, pathophysiology, and management. 331 Jun 37


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