Beta-blockade and exercise capacity in patients with mitral stenosis in sinus rhythm.

BACKGROUND AND AIM OF THE STUDY: The study aim was to determine whether beta-blocker treatment (atenolol) improves cardiopulmonary exercise performance and ventilatory response in patients with mitral stenosis in sinus rhythm. METHODS: A prospective study comparing the results of cardiopulmonary exercise tests (CPETs) was performed before and after atenolol therapy in 17 patients in NYHA classes I and II with mitral stenosis in sinus rhythm. Transthoracic echocardiography was performed pre-study, and left ventricular diameters, ejection fraction and mitral valve area monitored. CPETs (Naughton protocol) were performed by two different investigators before and after one-week atenolol therapy (50 mg/day). The second investigator was blinded to the result of the baseline test. O2 consumption, CO2 production, ventilatory parameters and respiratory exchange ratios were measured on line. RESULTS: Maximal O2 uptake (VO2max) did not differ significantly before and after beta-blockade (median 16.8 and 15.0 ml/kg/min, respectively. Median heart rate at rest (72 versus 55 beats/min; p = 0.0003) and during peak exercise (153 versus 105 beats/min; p = 0.0003), and anaerobic threshold (10 versus 8.9 ml/kg/min; p = 0.02) were lower with beta-blockade compared with the baseline state. Minute ventilation at maximum exercise (41 versus 40 l/min) and ventilatory equivalent for CO2 (34 versus 35) were unchanged with atenolol therapy, indicating no improvement in ventilatory performance. When patients were grouped into those in whom VO2max was improved with atenolol therapy (n = 7) and those in whom it was impaired (n = 10), there were no inter-group differences with respect to age, left ventricular function, severity of mitral stenosis, NYHA class and grade of beta-blockade reached. Four patients felt symptomatically worse during atenolol treatment (lower NYHA functional class). CONCLUSION: Beta-blockade does not improve exercise tolerance in patients with mitral stenosis in sinus rhythm. In addition, ventilatory performance does not change with treatment.

Dispersión del intervalo QT y variabilidad de la frecuencia cardíaca postinfarto. evolución temporal y relaciones con la función ventricular izquierda / QT interval dispersion and heart rate variability following myicardial infarction. Time course and relations with the left ventricular function

Introducción y objetivos. Se investigaron los cambios precoces en la dispersión del intervalo QT y variabilidad de la frecuencia cardíaca en un grupo de pacientes consecutivos hospitalizados por infarto de miocardio de cara anterior, así como el curso evolutivo de estos indicadores pronósticos durante un período de 6 meses y la relación entre estas variables y los parámetros de función ventricular izquierda. Métodos. Se estudiaron 42 pacientes consecutivos ingresados por infarto de miocardio de cara anterior con onda Q. Se llevaron a cabo en la primera semana y a los 6 meses postinfarto un análisis de la variabilidad de la frecuencia cardíaca (Holter de 24 horas) empleando el método de la demodulación compleja, una medida de la dispersión del intervalo QT en el electrocardiograma (ECG) estándar de 12 derivaciones (QT máximo - QT mínimo) y se obtuvieron los parámetros de función ventricular izquierda a partir de la ventriculografía de contraste y la extensión de la disfunción regional ventricular izquierda. Resultados. La dispersión del QT disminuyó significativamente entre la primera semana (0,07s [0,050,08]) y los 6 meses (0,06s [0,04-0,08], p =0,029); la extensión de la anormalidad de la motilidad parietal mostró una tendencia similar (desde 51 por ciento [27-56] hasta 33 por ciento [11-46], p<0,00001). En cambio, la desviación estándar de los ciclos RR aumenta entre la 1ª semana (31 ms [22-44]) y los 6 meses (43 ms [32-58], p< 0,00001). Sin embargo, la fracción de eyección ventricular izquierda, volumen telediastólico, y volumen telesistólico (46 ml/m2 [31-67] no mostraron cambios significativos en este período de tiempo. En la 1ª semana, la desviación estándar (r = 0,46, p< 0,01) y el ciclo RR medio (r = 0,59, p < 0,0001) se relacionaron con la fracción de eyección, Sin embargo, la dispersión de QT no se correlacionó con la variabilidad de la frecuencia cardíaca o los parámetros de función ventricular en la primera semana o a los 6 meses de evolución. No existieron diferencias en los parámetros autonómicos o hemodinámicos entre los pacientes que presentaron unos valores de dispersión del QT < 0,08 (n=15) o 0,08 ( n=16) segundos. Conclusiones. a) La dispersión del QT disminuye y la variabilidad de la frecuencia cardíaca aumenta en los primeros meses postinfarto; b) la disminución de la variabilidad de la frecuencia cardíaca tiende a ser mayor cuanto mayor es el deterioro de la función ventricular secundario al infarto; y c) no se han encontrado relaciones entre la dispersión del QT y las características clínicas, variabilidad de la frecuencia cardíaca o parámetros de función ventricular izquierda en la primera semana o a los 6 meses postinfarto (AU)

[QT interval dispersion in hospital patients admitted with cardiac insufficiency. Determinants and prognostic value]. / Dispersión del intervalo QT en pacientes ingresados por insuficiencia cardíaca. Determinantes y valor pronóstico.

INTRODUCTION AND OBJECTIVES: The determinants and the prognostic value of the QT interval dispersion are analysed in a group of consecutive patients admitted to hospital with heart failure. METHODS: One hundred twenty-two consecutive patients admitted because of heart failure in whom a reliable measurement of QT dispersion in the first electrocardiogram was obtained (maximum QT-minimum QT) were studied. The main clinical, analytic and echocardiographic data were recorded. A control group (n = 35) matched in age and sex with the study group was also analysed. RESULTS: The study group showed a greater QT dispersion than the control group (62 +/- 30 vs 40 +/- 21 ms; p = 0.01). Those cases with a QT dispersion > 80 ms (n = 50; 41%) exhibited a lower natremia (138 +/- 6 vs 141 +/- 4 mEq/l; p = 0.01), a higher probability of ischemic aetiology (52 vs 33%; RR = 2.2; IC95% 1.05-4.7; p = 0.04), an increased mortality during the first year (20 vs 6%; RR = 4.7; IC95% 1.3-16; p = 0.01) and during the whole follow-up (38 vs 19%; RR = 3.4; IC95% 1.3 a 8.6; p = 0.01) than those patients with a QT dispersion < 80 (n = 72; 59%). There were no significant differences between both groups with regard to the clinical, analytic or echocardiographic data. In the multivariate analysis only the ischemic etiology (p = 0.002) and the NYHA grade (p = 0.02) were related to a greater mortality. CONCLUSIONS: Patients with heart failure show an increased QT interval dispersion. This parameter is a simple tool that suggests an ischemic etiology and can help in prognosis stratification.

[Auricular fibrillation and stroke in patients with sick sinus syndromeusing permanent pacemakers]. / Fibrilación auricular y accidente vascular encefálico en pacientes con enfermedad del nodo sinusal portadores de marcapasos definitivos.

INTRODUCTION AND OBJECTIVES: Since physiological pacing systems have become available, a debate has raged about the merits of atrial versus ventricular pacing in the sick sinus syndrome. The goal of this retrospective report was to study the long term incidence and the independent predictors for atrial fibrillation and stroke in 153 paced patients with sick sinus syndrome, adjusting for differences in baseline clinical variables with multivariate analysis. METHOD AND RESULTS: From 1980 to 1994, we implanted 32 dualchamber, 33 atrial, and 88 ventricular pacemakers to treat patients with sick sinus syndrome. After a maximum follow-up of 177 months (median 30 months for paroxismal atrial fibrillation, 45 months for chronic atrial fibrillation and 43,5 months for stroke) the actuarial incidence of paroximal atrial fibrillation was 7.8% at 1 year, 29% at 5 years and 42% at 10 years. The actuarial incidence of chronic atrial fibrillation was 1.3% at 1 year, 9.8% at 5 years and 22% at 10 years. Independent predictors for paroxismal AF from Cox's model was history of atrial tachyarrhythmias (p < 0.0001), chronic obstructive pulmonary disease (p = 0,006) and age (> 70 years-old) (p = 0.035). Only a history of atrial tachyarrhythmias before pacemaker implant was an independent predictor for chronic atrial fibrillation (p < 0.0001). The odd ratio for paroxismal atrial fibrillation in patients with previous atrial tachyarrhythmias and chronic atrial fibrillation were 6 (2.8-12) and 4 (1.6-9.7) (95% confiance limits). Actuarial incidence of stroke was 3% at 1 year, 10% at 5 years and 14% at 10 years. Independent predictors for stroke were history of peripheral vascular disease (p = 0.033) and hypertensive cardiomyopathy (p = 0.015). Development of paroxysmal and chronic atrial fibrillation during the follow-up were higher in patients with stroke (p < 0.001 and p < 0.05). CONCLUSIONS: Development of atrial fibrillation and stroke in paced patients with sick sinus syndrome are strongly determined by clinical variables. Preimplant paroxysmal atrial tachyarrhythmias is the most important predictor for atrial fibrillation in the follow-up.