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Biomedical subjects

J R Carmona

Publications and source records attributed to J R Carmona.

10 recordsLinked to original sources

Mechanisms of sustained ventricular tachycardia in myotonic dystrophy: implications for catheter ablation.

BACKGROUND: Ventricular arrhythmias have been documented and linked to the high incidence of sudden death seen in patients with myotonic dystrophy. However, their precise mechanism is unknown, and their definitive therapy remains to be established. METHODS AND RESULTS: We studied 6 consecutive patients with myotonic dystrophy and sustained ventricular tachycardia by means of cardiac electrophysiological testing. Particular attention was paid to establish whether bundle-branch reentry was the tachycardia mechanism, and when such was the case, radiofrequency catheter ablation of either the right or left bundle branch was performed. Clinical tachycardia was inducible in all patients and had a bundle-branch reentrant mechanism. In 1 patient, 2 other morphologies of sustained tachycardia were also inducible, neither of which had ever been clinically documented, and both had a bundle-branch reentrant mechanism. Ventricular tachycardia was no longer inducible after bundle-branch ablation, except for a nonclinically documented and nonsustained ventricular tachycardia in the only patient who had apparent structural heart disease. CONCLUSIONS: A high clinical suspicion of bundle-branch reentrant tachycardia is justified in patients with myotonic dystrophy who exhibit wide QRS complex tachycardia or tachycardia-related symptoms. Because catheter ablation will easily and effectively abolish bundle-branch reentrant tachycardia, myotonic dystrophy should always be considered in patients with sustained ventricular tachycardia. This is especially true if no apparent heart disease is found.

Adult↗

Supraventricular arrhythmia as the cause of sudden death in hypertrophic cardiomyopathy.

Electrophysiological studies with simultaneous echocardiographic control and invasive measurement of intravascular pressures were carried out in a 13-year-old boy with hypertrophic cardiomyopathy who was hospitalized after an episode of aborted sudden death. Ventricular stimulation did not induce ventricular tachycardia, but atrial stimulation induced atrial fibrillation, atrial flutter and non-sustained ventricular tachycardia. Atrial stimulation (S1) at 200 beats.min-1 (10-15 s) also induced significant repolarization abnormalities in the 5-10 post-stimulation beats. Akinesia of the ventricular septum and posterior wall without opening of the mitral valve was documented by echocardiography. A complete anterior systolic motion, not observed under basal conditions, was detected in the first post-stimulation beat. Atrial stimulation at rates over 120 beats.min-1 caused a drop in systolic blood pressure, a rise in pulmonary artery pressure, and a decrease in cardiac output. Despite therapy with propranolol and amiodarone, the patient died suddenly.

Adolescent↗

[Long-term effects of captopril versus nifedipine retard on the lipid profile of mild to moderate normolipidemic essential hypertension patients. In representation of the Eastern Andalouz Cooperative Study].

The aim of the study was to evaluate the long-term (12 months) effects of captopril and nifedipine retard on the lipid profile of the non obese, non diabetic and normolipemic essential hypertensives. In a multicenter, randomised, open study we included 185 mild-moderate essential hypertensives responders to captopril (n = 96) or nifedipine retard (n = 89) in monotherapy, and with a total cholesterol between 200-239 mg/dl. No dietetic recommendations were given to the patients, except for moderate salt restriction. After 1 year follow-up, our results show that both drugs improved the lipid profile of the hypertensives. Patients with nifedipine retard showed a statistical significant decrease in the level of the total and LDL cholesterol and apoprotein B; while total and LDL cholesterol, triglycerides and apoproteins significantly decreased in the group treated with captopril. The possible pharmacological mechanisms involved in these beneficial effects are discussed; concluding that these properties made much more attractive these drugs to be used as first step therapy in the essential hypertensives.

Adult↗

Cardiac echinococcosis and systemic embolism. Report of a case.

We report the case of a 13-year-old boy who, previously in a healthy condition, was admitted to hospital with an acute ischemia of the lower half of the trunk following a slight traumatism. During the surgical operation it was noticed that the embolized material corresponded to hydatid vesicles. The patient died as a result of irreversible anaphylactic shock after the operation. The autopsy revealed the presence of a hydatid cyst in the posterior wall of the left atrium which had ruptured into the atrial cavity. The immediate exeresis of the cardiac cyst is suggested, when it is noticed that the embolized material is made up of hydatid vesicles located in the left cavities of the heart.

Adolescent↗

[Intramyocardial dissecting haematoma: an unusual form of cardiac rupture].

The intramyocardial dissecting haematoma is an unusual rupture of the left ventricular wall, complicating acute myocardial infarction. The mechanism is an hemorrhagic dissection among the spiral myocardial fibres creating a neocavitation limited by the myocardium. It appears in 9% of left ventricular wall ruptures, complicating acute myocardial infarction. Diagnosis is often difficult and in most of the cases it is post-mortem. We present the case report of a 69 year old patient who suffered a posterolateral acute myocardial infarction treated with primary PTCA/Stent plus AAS, clopidogrel, unfractioned heparin bolus and GP IIb- IIIa inhibitors. In the following few hours he suffered this unusual form of cardiac rupture that took him into cardiogenic shock and finally led to his death. The pathophysiology, diagnosis and management of this lethal complication of acute myocardial infarction (90% mortality in the medically treated group) which is only effectively treated by surgery are also reviewed.

Aged↗

[Sudden death in a normal heart. Idiopathic ventricular fibrillation. Review of the literature concerning one case].

Idiopathic ventricular fibrillation is that which is produced in the absence of structural cardiac disease and of other identifiable causes of ventricular fibrillation such as cardiotoxicity, electrolytical alterations or hereditary predisposition. The case of a healthy male, aged 37, who was asymptomatic until the day he was admitted to hospital where he showed numerous episodes of ventricular fibrillation without any previous triggering, is discussed. In the examination no cause was found to explain this, and an automatic defibrillator was implanted. The requirements for its diagnosis, risk stratification and the usefulness of the tests employed, as well as the treatments proposed are discussed.

Adult↗