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)

Coronary spasm provocation by intracoronary methylergonovine was performed in 14 patients (8 men and 6 women, mean age 56 +/- 6 years) with syncope that remained unexplained despite neurologic and noninvasive cardiac evaluations. Electrophysiologic testing was also performed in 6 of 14 patients. No patient had structural heart disease or significant fixed stenosis of greater than or equal to 75% in the coronary arteries. Six patients had no history of chest pain even when they developed syncope. Serious arrhythmia was documented in 2 patients, cardiac standstill in 1 and complete atrioventricular block in the other. Coronary spasm was induced in 9 patients using the methylergonovine provocation test. Multivessel spasms were found in 3 patients. Coronary spasm was induced in the artery supplying the inferior wall in 7 of 9 patients with positive results. In 4 of 9 patients who had a positive result, there was no prior history of chest pain. In 1 patient, whose electrocardiogram was recorded during syncope, cardiac standstill was documented and cardiac standstill and syncope also occurred during the provocation test. Monomorphic ventricular tachycardia was not induced by the electrophysiologic study. These results suggest that coronary spasm is involved in unexplained syncope.
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PMID:Possible role of coronary artery spasm in unexplained syncope. 231 52

Thirty-five patients with bundle branch block (BBB) and unexplained syncope underwent electrophysiologic study (EPS) including programmed ventricular stimulation and ajmaline administration (1 mg/kg, IV) to induce infra-His block. A prolonged HV interval (greater than 55 ms) was present in 16 of the 35 patients. Ajmaline-induced HV block occurred in 12 patients (complete HV block in 10, and 2:1 HV block in two). Monomorphic ventricular tachycardia (VT) was inducible in nine (25.7%) and polymorphic VT in two patients (5.7%). Left ventricular ejection fraction (LVEF) was less than 40% in five patients (45.5%) with inducible VT. Two patients had an unexpected co-existence of inducible HV block and VT. The remaining 14 patients (40%) had no detectable abnormality. The incidence of inducible VT was higher (45% vs 13.3%), and the presence of negative studies was lower (30% vs 53.3%) in patients with structural heart disease (n = 20), when compared to those with no significant heart disease (n = 15) (differences not significant [NS]). During a mean follow-up period of 16.5 +/- 9.2 months, all the patients with inducible HV block have been asymptomatic after having received permanent pacemakers. Patients with inducible monomorphic VT (except one with poor left ventricular function who died suddenly) have also been asymptomatic on antiarrhythmic drugs. Of the remaining patients, seven with normal EPS, two with prolonged HV intervals but no inducible HV block (despite being given permanent pacemakers) and one patient with polymorphic VT on antiarrhythmic drugs continue to have recurrent syncope. Approximately 60% of patients with BBB and unexplained syncope have clinically significant electrophysiologic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of patients with bundle branch block and "unexplained" syncope: a study based on comprehensive electrophysiologic testing and ajmaline stress. 245 15

Results of recent clinical trials allow an evidence-based approach to ventricular arrhythmias (VAs). The implantable cardioverter-defibrillator (ICD) has clearly established its role in the secondary prevention of VA and should be considered first-line therapy in patients surviving episodes of potentially lethal VAs. It has also been clearly shown that in these patients, antiarrhythmic drug selection by means of serial Holter recording or electrophysiologic study does not improve survival. Antiarrhythmic drug therapy (including amiodarone) as primary prevention in high-risk patients (eg, those who have experienced a myocardial infarction or who have heart failure) has thus far not reduced the mortality rate. In contrast, use of the ICD as a primary preventative strategy has reduced the mortality rate in patients after myocardial infarction who have reduced left ventricular function, nonsustained ventricular tachycardia, and inducible ventricular tachycardia during electrophysiologic study. Thus, patients fitting this clinical profile are best served by implantation of an ICD. Monomorphic ventricular tachycardia occurs rarely in patients without heart disease. These arrhythmias are best treated with catheter ablation therapy, a treatment with a high rate of success and a low rate of complications.
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PMID:Ventricular Arrhythmias. 1109 37

Monomorphic ventricular tachycardia (MVT) is well described in patients who have had a ventricular scar due to repair of congenital heart disease. A 54-year-old woman presented with MVT 20 years after WPW surgery for a left-sided accessory pathway. The circuit was mapped to an area at the base of the left ventricle consistent with the incision described in the operation report. Entrainment confirmed the re-entrant circuit. Successful radiofrequency ablation was performed in a zone of slowed conduction consistent with the circuit isthmus. Any iatrogenic ventricular scar may form the substrate for MVT and be treated with standard electrophysiology techniques.
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PMID:Monomorphic ventricular tachycardia related to Wolff-Parkinson-White surgery. 1727 35

Monomorphic ventricular tachycardia (VT) is a unique manifestation of hyperthyroidism. We present the case of a 41-year-old male with a history of hyperthyroidism presenting with palpitations secondary to non-sustained episodes of monomorphic VT. Cardiac arrhythmias due to thyrotoxicosis are perpetually supraventricular in origin. Monomorphic VT in the setting of thyrotoxicosis in the absence of structural heart disease is exceedingly rare. After starting propranolol and increasing the dose of methimazole, the patient had no further episodes of VT. It is important to recognize repetitive monomorphic VT as an understated but important manifestation of thyrotoxicosis. Propranolol is associated with an excellent response in these patients and anti-thyroid medications such as methimazole effectively reverse thyrotoxicity.
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PMID:Repetitive monomorphic ventricular tachycardia as a manifestation of suboptimally treated thyrotoxicosis. 2202 38

Monomorphic ventricular tachycardia is basically a benign phenomenon in patients without structural heart disease. The focal source of the tachycardia is usually located in the right ventricular outflow tract and more rarely in the left ventricular outflow tract. Aortic sinus of Valsalva (ASV) is a well-known source of atrial and ventricular tachycardias. We report a case with simultaneous existence of sustained atrial and ventricular tachycardias originating from ASV, which was successfully treated with radiofrequency catheter ablation.
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PMID:Simultaneous existence of sustained double chamber tachycardias originating from the aortic sinus of Valsalva. 2208 42

Nonpenetrating, blunt chest trauma is a serious medical condition with varied clinical presentations and implications. This can be the result of a dense projectile during competitive and recreational sports but may also include other etiologies such as motor vehicle accidents or traumatic falls. In this setting, the manifestation of ventricular arrhythmias has been observed both acutely and chronically. This is based on two entirely separate mechanisms and etiologies requiring different treatments. Ventricular fibrillation can occur immediately after chest wall injury (commotio cordis) and requires rapid defibrillation. Monomorphic ventricular tachycardia can develop in the chronic stage due to underlying structural heart disease long after blunt chest injury. The associated arrhythmogenic tissue may be complex and provides the necessary substrate to form a reentrant VT circuit. Ventricular tachycardia in the absence of overt structural heart disease appears to be focal in nature with rapid termination during ablation. Regardless of the VT mechanism, patients with recurrent episodes, despite antiarrhythmic medication in the chronic stage following blunt chest injury, are likely to require ablation to achieve VT control. This review article will describe the mechanisms, pathophysiology, and treatment of ventricular arrhythmias that occur in both the acute and chronic stages following blunt chest trauma.
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PMID:Mechanisms and Clinical Management of Ventricular Arrhythmias following Blunt Chest Trauma. 2698 8