ABSTRACT
Tachycardia-induced cardiomyopathy is an entity characterized by reversible dysfunction of the left ventricle, which can be induced by different types of arrhythmia such as atrial fibrillation, atrial flutter, incessant supraventricular tachycardia and ventricular arrhythmia (more frequent causes). Correct identification of the causative arrhythmia and normalization of the heart rate (e.g through medical treatment, electrical cardioversion, ablation) can lead to recovery of left ventricular function. Tachycardia-induced cardiomyopathy should be suspected in patients with tachycardia and left ventricular dysfunction (heart failure setting), especially when there is no history of previous heart disease. Its usual phenotype is that of non-ischaemic/non-valvular dilated cardiomyopathy and it can occur in both children (main cause: permanent junctional reciprocating tachycardia) and adults (main cause: atrial fibrillation). With proper treatment, most cases recover within a few months, though there is a risk of relapse, especially when the causal arrhythmia reappears or its control is lost. This is a narrative review that comprehensively addresses the pathophysiology, clinical manifestations, and therapeutic management of tachycardia-induced cardiomyopathy. This article is part of the Emerging concepts in heart failure management and treatment Special Issue: https://www.drugsincontext.com/special_issues/emerging-concepts-in-heart-failure-management-and-treatment.
ABSTRACT
BACKGROUND: Diagnosing non-ST-segment elevation acute coronary syndrome (NSTE-ACS) is not always straightforward. Left ventricular global longitudinal strain (LVGLS) is an echocardiographic method capable of detecting subclinical regional and global ventricular contractile dysfunction due to myocardial ischemia. The objectives of this study were to evaluate the efficacy of LVGLS in diagnosing severe coronary disease in patients with chest pain suggestive of NSTE-ACS and to assess the relationships between LVGLS reduction and ultrasensitive troponin T (UsTnT) elevation, electrocardiographic changes suggestive of ischemia, and the number of vessels with severe obstructions. METHODS: This prospective, observational study evaluated hospitalized patients with chest pain of presumed coronary etiology. All patients underwent electrocardiography (ECG), UsTnT measurement, Doppler echocardiography, LVGLS measurement, and coronary angiography Coronary angiogram (CA) within 48 h of hospitalization. RESULTS: A total of 75 patients with a mean age of 58 ± 17 years were included, of whom 84% (63 patients) were men. An LVGLS value of <-16.5, as determined by the Youden index proved to be useful for the detection of severe coronary obstructions (lesions >70%). The sensitivity, specificity, and positive and negative predictive values were 96%, 88%, 92%, and 92%, respectively. The number of coronary arteries involved had a direct relationship with the degree of LVGLS reduction (P < 0.001). Elevated UsTnT levels occurred more frequently in patients with reduced LVGLS than in those with normal LVGLS (83% vs. 17%, P < 0.0001). Abnormal strain was not associated with electrocardiographic changes suggestive of ischemia. CONCLUSIONS: LVGLS measurement in patients with presumed NSTE-ACS is efficient in predicting the presence of severe coronary disease. The number of coronary arteries involved has a direct relationship with the degree of LVGLS reduction. Abnormal strain is associated with UsTnT elevations but not with electrocardiographic changes suggestive of ischemia.
ABSTRACT
Introducción. La cafeína es una de las sustancias más consumidas mundialmente. Sus efectos fisiológicos han generado preocupación sobre sus potenciales efectos perjudiciales a nivel cardiovascular. Objetivos. Determinar el efecto de dosis habituales de cafeína (50 mg) sobre variables hemodinámicas valoradas con el Mobil-O-GRAPH PWA en sujetos sanos. Evaluar si el tabaquismo exacerba el efecto del café sobre estos parámetros. Materiales y métodos. Estudio prospectivo. Se incluyeron sujetos sanos entre 18 y 55 años, de ambos sexos que debían estar 12 horas libres de cigarrillos o de sustancias con cafeína. Se obtuvieron medidas de parámetros hemodinámicos con el Mobil-O-GRAPH PWA antes y a los 0, 30 y 60 minutos del consumo de 140 mL de café con 50 mg de cafeína. Se evaluó si el tabaquismo exacerba el efecto de la cafeína sobre estos parámetros vasculares. Resultados. Se incluyeron 27 pacientes de los cuales el 45% fue de sexo masculino, con una edad media de 33 ± 9 años. El 29% de los pacientes era tabaquista. A los 60 minutos de la ingesta de café se observó un incremento de 3 mm Hg de la presión arterial media (PAM) que fue significativa (p=0,03). Comparado a los no fumadores, los tabaquistas mostraron un incremento más marcado de la PAM (9 mm Hg vs 2 mm Hg; p=0,05). Los otros parámetros fueron similares en ambos grupos. Conclusión. En sujetos sanos la ingesta de 50 mg de café incrementa la PAM en 3 mm Hg a los 60 minutos y este efecto es más marcado en tabaquistas.
Introduction. Caffeine is one of the most consumed substances worldwide. Its physiological effects have been generated concerns about its potential harmful effects at the cardiovascular level. Objectives. To determine the effect of usual doses of caffeine (50mg) on hemodynamic variables assessed with the Mobil-O-GRAPH PWA in healthy subjects. To assess if smoking exacerbates the effect of coffee on these parameters. Materials and methods. Prospective study. We included healthy subjects between 18 and 55 years of age, of both sexes who had to be 12 hours free of cigarettes or substances with caffeine. Measurements of hemodynamic parameters were obtained with the Mobil-O-GRAPH PWA before and at 0, 30 and 60 minutes of the consumption of 140 mL of coffee with 50 mg of caffeine. It was evaluated if smoking exacerbates the effect of caffeine on these vascular parameters. Results. We included 27 patients of which 45% were male, with a mean age of 33 ± 9 years. The 29% of the patients were smokers. At 60 minutes of coffee intake, an increase of 3 mm Hg in mean arterial pressure (MAP) was observed, which was significant (p = 0.03). Compared to non smokers, smokers showed a more marked increase in MAP (9 mm Hg vs 2 mm Hg, p = 0.05). The other parameters were similar in both groups. Conclusion. In healthy subjects the intake of 50 mg of coffee increases the MAP by 3mmHg at 60 minutes and this effect is more marked in smokers.
Introdução. A cafeína é uma das substâncias mais consumidas no mundo. Seus efeitos fisiológicos geraram preocupação sobre os seus efeitos nocivos potenciais ao nível cardiovascular. Objetivos. Determinar o efeito de doses usuais de cafeína (50mg) nas variáveis hemodinâmicas avaliadas com o Mobil-O-GRAPH PWA em indivíduos saudáveis. Avaliar se o ato de fumar exacerba o efeito do café nesses parâmetros. Materiais e métodos. Estudo prospectivo. Foram incluídos indivíduos saudáveis entre 18 e 55 anos de idade, de ambos os sexos, que deveriam ter 12 horas livres de cigarros ou substâncias com cafeína. As medidas dos parâmetros hemodinâmicos foram obtidas com o Mobil-O-GRAPH PWA antes e aos 0, 30 e 60 minutos do consumo de 140 mL de café com 50 mg de cafeína. Foi avaliado se fumar exacerba o efeito da cafeína sobre esses parâmetros vasculares. Resultados. Foram incluídos 27 pacientes, dos quais 45% eram do sexo masculino, com média de idade de 33 ± 9 anos. O 29% dos pacientes eram fumantes. Aos 60 minutos de ingestão de café, observou-se um aumento de 3 mm Hg na pressão arterial média (PAM), que foi significativo (p=0,03). Em comparação com os não-fumantes, os fumantes apresentaram um aumento mais acentuado da PAM (9 mm Hg vs 2 mm Hg, p=0,05). Os outros parâmetros foram semelhantes nos dois grupos. Conclusão. Em indivíduos saudáveis, a ingestão de 50 mg de café aumenta a PAM em 3 mm Hg aos 60 minutos e esse efeito é mais acentuado nos fumantes.
