Subclinical Left Ventricular Systolic Dysfunction in Hospitalized Patients with COVID-19 by Strain: A 30-Day Echocardiographic Follow-Up.

Background and Objectives: Available studies confirm myocardial injury and its association with mortality in patients with COVID-19, but few data have been reported from echocardiographic studies. The aim of this study was to identify subclinical left ventricular dysfunction by global longitudinal strain (GLS) and its evolution in the short term in hospitalized patients with COVID-19. Materials and Methods: Thirty-one consecutive noncritical patients admitted for COVID-19 were included. Information on demographics, laboratory results, comorbidities, and medications was collected. Transthoracic echocardiograms were performed using a Philips Affinity 50, at the acute stage and at a 30-day follow-up. Automated left ventricular GLS was measured using a Philips Qlab 13.0. A GLS of <-15.9% was defined as abnormal. Results: The mean age was 65 ± 15.2 years, and 61.3% of patients were male. Nine patients (29%) had elevated levels of high-sensitivity troponin I. Left ventricular ejection fraction was preserved in all; however, 11 of them (35.5%) showed reduced GLS. These patients had higher troponin levels (median, 23.7 vs. 3.2 ng/L; p < 0.05) and NT-proBNP (median, 753 vs. 81 pg/mL; p < 0.05). The multivariate analysis revealed that myocardial injury, defined as increased troponin, was significantly associated with GLS values (coefficient B; p < 0.05). Follow-up at 30 days showed an improvement in GLS values in patients with subclinical left ventricular dysfunction (-16.4 ± 2.07% vs. -13.2 ± 2.40%; p < 0.01), without changes in the normal GLS group. Conclusions: Subclinical left ventricular dysfunction is common in noncritical hospitalized patients with COVID-19 (one in every three patients), even with preserved left ventricular ejection fraction. This impairment tends to be reversible on clinical recovery.

Etiology and Programming Effects on Shock Efficacy in ICD Recipients.

BACKGROUND: We sought to assess the efficacy of high-energy shocks to restore rhythm and predictors of success in patients with sustained ventricular arrhythmias and implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Data from 162 patients included in the UMBRELLA study that experienced one or more episodes of ventricular tachycardia (VT) for which ICD shocks of at least 30 Joules were delivered (appropriate high-energy shocks) were analyzed. In total, 456 ventricular arrhythmia episodes were registered. Forty four episodes (9.6%) from 39 patients (24%) had at least one ineffective high-energy shock delivered. Hypertrophic cardiomyopathy was more frequent among patients with unsuccessful shocks (10.3% vs 2.4%). Patients with ineffective shocks had higher proportion of sustained monomorphic ventricular arrhythmias (86.4%; the other 13.6% were sustained polymorphic and ventricular fibrillation [VF]) compared with patients with all their shocks effective (62.9%, P = 0.02). No statistical differences were found between groups in time from detection to the high-energy shock delivery, in tachycardia cycle length, or in antitachycardia pacing, but patients with ineffective high-energy shocks had higher proportion of previously ineffective low-energy shock (9.1% vs 0.5%, P = 0.01). CONCLUSION: We found a substantial rate of ineffective high-energy shocks for the treatment of VT or VF in patients with ICD. High-energy shock efficacy seems to be reduced by hypertrophic cardiomyopathy and by the administration of previous low-energy shocks.

Narrow irregular QRS tachycardia with AV dissociation: what is the mechanism?

A 39-year-old woman with no structural heart disease and frequent episodes of sudden onset palpitations was referred for the electrophysiological study. During the study, a slightly irregular narrow QRS tachycardia with AV dissociation was repeatedly induced and spontaneously terminated. Apparently, irregular cycles and termination of the tachycardia were related to the dissociated sinus rhythm: atrial depolarizations timed when the AV junction was refractory were able to reset the tachycardia, while early atrial depolarizations caused its termination. This observation was enough to diagnose the tachycardia mechanism in our case.

Time-to-Effect-Based Dosing Strategy for Cryoballoon Ablation in Patients With Paroxysmal Atrial Fibrillation: Results of the plusONE Multicenter Randomized Controlled Noninferiority Trial.

BACKGROUND: The optimal dosage of cryotherapy during cryoballoon ablation of pulmonary veins is still unclear. This trial tested the noninferiority of a novel, individualized, cryotherapy-dosing strategy for each vein. METHODS AND RESULTS: This prospective, randomized, multicenter, noninferiority study included 140 patients with paroxysmal atrial fibrillation, which was refractory to antiarrhythmic drugs. Patients were randomly assigned to a conventional strategy of 180-second cryoballoon applications per vein with a bonus freeze (control group, n=70) or to a shorter-time application protocol, with 1 application that lasted the time required for electric block time to effect plus 60- and a 120-second freeze bonus (study group, n=70). Patients were followed with a long-term monitoring system of 30 days. At 1-year follow-up, no difference was observed in terms of free atrial fibrillation-recurrence rates: 79.4% in control versus 78.3% in study group (Δ=1.15%; 90% confidence interval, -10.33% to 12.63%; P=0.869). Time to effect was detected in 72.1% of veins. The control and study groups had similar mean number of applications per patient (9.6±2 versus 9.9±2.4; P=0.76). Compared with controls, the study group had a significantly shorter cryotherapy time (28.3±7 versus 19.4±4.3 minutes; P<0.001), left atrium time (104±25 versus 92±23 minutes; P<0.01), and total procedure time (135±35 versus 119±31 minutes; P<0.01). No differences were observed in complications or acute reconnections. CONCLUSIONS: The new time-to-effect-based cryotherapy dosage protocol led to shorter cryotherapy and procedure times, with equal safety, and similar acute and 1-year follow-up results, compared with the conventional approach. CLINICAL TRIAL REGISTRATION: URL: https://clinicaltrials.gov. Unique identifier: NCT02789358.

Quality of Anticoagulation With Vitamin K Antagonists.

BACKGROUND: Vitamin K antagonists (VKA) have a narrow therapeutic range, and literature analysis reveals poor quality of anticoagulation control. We sought to assess the prevalence of poor anticoagulant control in patients under VKA treatment in the prevention of stroke for atrial fibrillation (AF). HYPOTHESIS: Control of anticoagulation with VKA is inadequate in a high percentage of patients with AF. METHODS: Patients with AF under VKA treatment were prospectively recruited in this observational registry. The sample comprised 948 patients. The estimated time spent in the therapeutic range (TTR) was calculated, and variables related with a TTR >65% were analyzed. RESULTS: Mean age was 73.8 ± 9.4 years, and 42.5% of the patients were women. Mean TTR was 63.77% ± 23.80% for the direct method and 60.27% ± 24.48% for the Rosendaal method. Prevalence of poor anticoagulation control was 54%. Variables associated with good anticoagulation control were university studies (odds ratio [OR]: 1.99, 95% confidence interval [CI]: 1.08-3.64), chronic hepatic disease (OR: 8.15, 95% CI: 1.57-42.24), low comorbidity expressed as Charlson index (OR: 0.87, 95% CI: 0.76-0.99), no previous cardiac disease (OR: 0.64, 95% CI: 0.41-0.98), lower risk of bleeding assessed as hypertension, abnormal renal/liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly age, and use of drugs or alcohol (HAS-BLED; OR: 0.81, 95% CI: 0.69-0.95), and lower heart rate (OR: 0.99, 95% CI: 0.98-0.99). CONCLUSIONS: Patients who receive VKA to prevent stroke for AF spend less than half the time within therapeutic range.

Valor pronóstico de la enfermedad arterial periférica en la cardiopatía isquémica / Prognostic implications of peripheral arterial disease for ischemic heart disease

La aterosclerosis es un proceso fisiopatológico progresivo que puede afectar simultáneamente a múltiples territorios vasculares y tiene origen en diversos factores como la diabetes mellitus, el tabaquismo, la hipertensión arterial o la dislipemia. Consecuentemente, la coexistencia de enfermedad arterial coronaria y enfermedad arterial periférica (EAP) es frecuente. Recientemente se han publicado datos que indican que la EAP en el paciente con enfermedad coronaria podría implicar un pronóstico peor que el meramente establecido por los factores de riesgo clásicos. Éstos señalan a la EAP como un marcador de riesgo independiente en los distintos subgrupos de pacientes con cardiopatía isquémica. Por lo tanto, la criba de EAP mediante el índice tobillo-brazo en esta población parece un paso obligado para detectar a pacientes en mayor riesgo e intensificar en ellos las medidas preventivas y terapéuticas de que disponemos (AU)

Atherosclerosis is a progressive pathophysiologic process that can simultaneously affect a number of different vascular beds and that can be caused by a range of factors such as diabetes mellitus, smoking, hypertension and dyslipidemia. Consequently, coronary artery disease and peripheral arterial disease (PAD) frequently coexist. Recently published data suggest that the presence of PAD in a patient with coronary artery disease implies a poorer prognosis than would be expected from classical risk factors alone. These findings indicate that PAD is an independent risk factor in different subgroups of patients with ischemic heart disease. Consequently, early diagnosis of PAD in these patients by measuring the ankle-brachial index would appear to be an essential step in identifying those at a high risk and in bringing about an increase in the use of currently available preventive and therapeutic measures in these patients (AU)

Situación de la enfermedad cardiovascular en España. Del riesgo a la enfermedad / Cardiovascular disease in Spain today. From risk factors to morbidity

La enfermedad cardiovascular es la primera causa de muerte en nuestro país pese a que la mayor parte de los factores de riesgo son conocidos y modificables. La pérdida de los hábitos cardiosaludables ha ralentizado la continua reducción de la mortalidad por cardiopatía isquémica durante los últimos años. Además, el aumento de los factores asociados al desarrollo de enfermedad cardiovascular durante las últimas décadas ya ha puesto en marcha los mecanismos patogénicos precisos que en unos años darán lugar a la aparición de eventos cardiovasculares en un porcentaje muy importante de la población española. El escaso control conseguido de determinados factores de riesgo hace que más de la mitad de la población española con algún factor conocido no cumpla los objetivos terapéuticos. La marcada prevalencia de estos predisponentes en el colectivo anciano, junto con el progresivo envejecimiento de la población, no hace más que acrecentar estos problemas y auguran un aumento de las enfermedades cardiovasculares cuyos límites todavía no conocemos (AU)

Cardiovascular disease is the leading cause of death in Spain. However, the majority of risk factors have been identified and are modifiable. In recent years, the loss of lifestyle habits that favor cardiovascular health has slowed the ongoing decline in mortality due to ischemic heart disease. Moreover, the increase in the incidence of factors associated with the development of cardiovascular disease that has occurred during the last few decades has already set in motion pathogenetic mechanisms that will, in the next few years, lead to the occurrence of cardiovascular events in a significant percentage of the Spanish population. Poor control of certain risk factors means that more than half the Spanish population with known risk factors does not achieve therapeutic objectives. The high prevalence of these predisposing factors in older people, coupled with the progressive aging of population, can only worsen the situation and presages a rise in the incidence of cardiovascular disease whose upper limit is still unknown (AU)