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X Viñolas

Publications and source records attributed to X Viñolas.

13 recordsLinked to original sources
PubMed2000

Gene-specific differences in the circadian variation of ventricular repolarization in the long QT syndrome: a key to sudden death during sleep?

BACKGROUND: In the long QT syndrome (LQTS) most life-threatening cardiac events occur in association with physical or emotional stress. However, a minority of patients dies suddenly during sleep; intriguingly, these sleep-related sudden deaths tend to cluster in families. The mechanism(s) underlying this phenomenon and the reason why it occurs in few selected families are unknown. Recently, some of the LQTS genes have been identified leading to three main subgroups (LQT1, LQT2, LQT3) associated respectively with mutations affecting the following ionic currents involved in the control of ventricular repolarization: I(Ks), I(Kr), I(Na). We have recently observed that cardiac events nighttime are rare in LQT1 and frequent in LQT3 patients. METHODS: We studied 26 LQTS patients all genotyped (11 LQT1, 9 LQT2, 6 LQT3) and 26 healthy controls matched by age and gender. Using a specific software, 24-hour ambulatory ECG recordings were performed and the QT interval was measured in order to allow comparison between QTc nighttime and daytime. RESULTS: The main finding is that while LQT1 patients show a trend for modest QTc shortening and LQT2 patients a trend for modest lengthening nighttime versus daytime, LQT3 patients show clear lengthening of the QTc nighttime. These changes are not explained by heart rate changes or by the use of beta-blockers. CONCLUSIONS: The marked tendency for further QT prolongation nighttime, which clearly increases arrhythmic risk, present among LQT3 patients and absent among LQT1 patients, provides an explanation for the gene-specific higher risk for sudden death during sleep for LQT3 compared to LQT1 patients.

Adolescent↗
PubMed2000

[Intermittent pre-excitation after adenosine administration].

We describe a case of 2:1 intermittent preexcitation after adenosine administration in a patient with an accessory pathway that did not show preexcitation on the basal ECG. We review the mechanisms involved that explain this event and the possible utility of adenosine to show accessory pathways that do not show preexcitation on the ECG.

Adenosine↗
PubMed1997

Automatic measurement of corrected QT interval in Holter recordings: comparison of its dynamic behavior in patients after myocardial infarction with and without life-threatening arrhythmias.

This study was designed to determine the value of automatic corrected QT-interval measurement in Holter tapes in patients after myocardial infarction as a marker of life-threatening ventricular arrhythmias. We compared the corrected QT interval, automatically measured in 24-hour Holter recordings, in two groups of patients after myocardial infarction: group I was composed of 14 patients admitted consecutively to our hospital for documented sustained ventricular tachycardia or out-of-hospital cardiac arrest. Group II consisted of 28 patients with previous myocardial infarction with characteristics similar to those of group I, but without malignant ventricular arrhythmias in the follow-up. The global mean 24-hour corrected QT interval was longer in group I (425 +/- 20 msec) than in those patients after myocardial infarction without arrhythmias (group II) (405 +/- 17 msec; p < 0.01). Furthermore, a significant proportion of patients of group I (seven of 14) exhibited more peaks of corrected QT longer than 500 msec compared with patients of group II (two of 28; p < 0.005). A circadian rhythm of corrected QT peaks was observed in group I, having a significantly higher incidence from 11 PM to 11 AM (p < 0.05). We conclude that automatic corrected QT-interval measurement on Holter electrocardiogram is now available and feasible. Our results suggest that this is a marker for risk assessment of life-threatening ventricular arrhythmias. Large-scale trials are needed to confirm these results and to determine the predictive value of this technique for risk stratification.

Algorithms↗
PubMed1995

Cardiac arrhythmias and left ventricular hypertrophy in systemic hypertension and their influences on prognosis.

Left ventricular hypertrophy (LVH) is the adaptative mechanism of the heart to systolic overload of the left ventricle. Nevertheless, LVH plays a role in some complications, such as cardiac arrhythmias. Patients with LVH are more likely to develop ventricular arrhythmias than the hypertensive population without LVH. Further, the relation between left ventricular mass and ventricular arrhythmias is graded and continuous. The arrhythmias described in hypertensive patients with LVH are usually isolated premature ventricular contractions. The presence of electrocardiographic criteria of LVH represents a risk of higher incidence of sudden death, especially in men. The risk is even greater in the presence of ventricular arrhythmias. The presence of late potentials has been recently characterized as more related to ventricular arrhythmias than LVH. Antihypertensive drugs that can reduce LVH also have a beneficial effect on cardiovascular morbility and mortality.

Antihypertensive Agents↗
PubMed1995

Electrocardiographic and clinical precursors of ventricular fibrillation: chain of events.

Ventricular fibrillation is the final event in the majority of cases of sudden death. The ECG and clinical precursors of ventricular fibrillation are discussed in this article. Ventricular fibrillation usually appears as a consequence of a chain of events that leads to the appearance of this lethal arrhythmia. We review the markers of the vulnerable myocardium prone to ventricular fibrillation, the triggers and modulators that act on this vulnerable myocardium, and the event(s) that constitute the final step preceding this arrhythmia. The final step may be as unique as a sudden waterfall or present as a cascade of successive phenomena.

Electrocardiography↗
PubMed1994

Risk stratification after myocardial infarction: role of electrical instability, ischemia, and left ventricular function.

The problem of risk stratification after myocardial infarction is reviewed. There are three major complications: new ischemic events, congestive heart failure, and malignant arrhythmias and sudden death, related to the presence of residual ischemia, left ventricular dysfunction, and electrical instability. The bidirectional interactions among these three factors is analyzed. The risk is in the middle of a triangle, the three angles of which are the above-mentioned factors. All the "satellite" factors that appear from all three angles are presented. Furthermore, the most important parameters and techniques employed to detect risk, multifactorial approach of risk stratification, and changes of risk stratification in the thrombolytic era are briefly reviewed.

Arrhythmias, Cardiac↗
PubMed1994

[Mechanisms favoring and triggering atrial fibrillation].

Many experimental and clinical studies have demonstrated that it is possible to trigger atrial fibrillation (AF) by vagal stimulation which reduces and disperses the atrial refractory periods and decreases the threshold of fibrillation. In order to induce fibrillation, it is necessary to deliver a stimulation near to the refractory period. It has also been shown that, in these conditions, there is a delay in atrial conduction. A temporal relationship between the preceding diastole and the coupling interval increases atrial vulnerability and plays an equally important role. The decrease in the effective atrial refractory period, especially when the values are widely dispersed, and the delay in conduction predisposing to atrial reentry, may be considered to be the two most important electrophysiological mechanisms of AF. However, in order to maintain AF, the atrium must be dilated, especially when there is a concurrent cardiac disease. The presence of a shorter "wave length" of activation allowing multiple reentry circuits is an essential condition for sustaining AF. All conductions of induction and maintenance of AF may be observed without participation of S.N.A.. When no cause of AF (atrial pathology, etc.) is apparent, a short atrial refractory period with dispersion of its values and slowing of atrial conduction in presence of an extrastimulus are the probable inducing factors.

Atrial Fibrillation↗