Prevalence and time course of arrhythmia-induced cardiomyopathy in patients with newly diagnosed heart failure and concomitant tachyarrhythmia - the TACHY-HF pilot trial

Background: Arrhythmias may often be a result of heart failure, but they can also cause left-ventricular systolic dysfunction (LVSD), thereby presenting as arrhythmia-induced cardiomyopathy (AIC). AIC-diagnosis is established retrospectively when LVSD normalizes or improves significantly over time following rhythm restoration. However, the prevalence and most importantly the time course of this relevant disease remain unclear and hence merit investigation to enable the correct diagnosis. Purpose: Therefore, our aim was to evaluate a) the occurrence of AIC in this clinical relevant cohort of patients with newly diagnosed and otherwise unexplainable LVSD and concomitant tachycardia and b) the time needed to fulfill the diagnostic criteria of AIC in order to facilitate a diagnostic algorithm. Method: We prospectively screened patients hospitalized for newly diagnosed and otherwise unexplainable LVSD (i.e. left ventricular ejection fraction (LVEF) <50%) and coexisting tachyarrhythmia (atrial fibrillation/flutter + heart rate (HR) >100/min) in 3 cardiological centers. Coronary angiography and cardiac magnetic resonance imaging were performed to exclude other causes for LVSD. Patients underwent a rhythm control strategy in accordance to the local clinical pathways. LVEF was assessed by echocardiography at presentation and at follow-up (FU) visits after 2, 4, and 6 months. Patients who lost sinus rhythm (SR) during FU were excluded. Patients with any increase of ≥15% in absolute EF or an EF ≥50% with an improvement of ≥10% after 6 months of FU were assigned to the AICgroup, which is a common definition of AIC. All others were assigned to an idiopathic DCM-group as final comparator. Results: 68 patients were eligible, 18 of them were excluded: 1 lost to follow-up, 1 PCI, 2 COVID-19, 1 diagnosed cancer, 1 withdraw consent and 12 lost SR. Thus, our sample consists of a total of 50 patients. At presentation, mean±SD HR was 121±17/min. After rhythm therapy, HR normalized (67±10/min) and LVEF increased in both groups, see fig. 1. Surprisingly, only 9 patients did not fulfill the AIC-criteria in this specific collective resulting in a prevalence of 82% (95%-CI: 68% - 92%). This high prevalence of AIC underlines the importance of the disease. 2 and 4 months after rhythm intervention, 58% and 73% of patients fulfilled AIC-criteria (fig. 2). The sensitivity for detection of AIC by echocardiographic LVEF-measurement at months 2 and 4 of FU was 65% and 86% with a specificity of 100%, emphasizing that a FU of 6 months is necessary to certainly distinguish between AIC and idiopathic DCM. Conclusion: The prevalence of AIC in patients with newly diagnosed and otherwise unexplainable LVSD with concomitant tachycardia is 82%. Analysis of the time course of AIC clearly suggests that the final diagnosis cannot be established before 6 months after successful rhythm restoration. These results may help to improve diagnosis of AIC in daily clinical practice.

SARS-CoV2 infection: Functional and morphological cardiopulmonary changes in elite handball players

Background: There is increasing evidence of cardiac involvement in SARS-COV-2 infections. This may not only apply to symptomatic infections but may also affect asymptomatic athletes. This study aimed to characterize the possible acute cardiac involvement of SARS-COV-2 infection in athletes both morphologically and functionally. Methods and results: Eight elite handball players (27±3.5 y) with past SARS-COV-2 infection were retrospectively analyzed and compared with four uninfected team-mates (22±2.6 y). Athletes were examined 19±7 d after positive PCR-test. Echocardiographic assessment of the global longitudinal strain under resting conditions was not significantly changed after SARS-CoV2 infection (-17.7% vs. -18.1%) but magnetic resonance imaging showed minor signs of acute inflammation/edema in all patients (T2-mapping: +4.1ms) without reaching the Lake-Louis criteria. Spiroergometric analysis showed a significant reduction in VO2max (-292 ml/min, -7.0%), oxygen-pulse (-2.4 ml/beat, -10.4%), and respiratory minute volume (VE) (-18.9 l/min, -13.8%) in athletes with a history of SARS-CoV2 infection (p<0.05, respectively). The parameters were unchanged in the control group. Conclusion: SARS-CoV2 infection caused functional impairment of cardiopulmonary performance primarily under stress in elite athletes. It seems reasonable to screen athletes after SARS-CoV2 infection at least with spiroergometry to mark performance limitations and to ensure an optimal return to competition.

SARS-CoV2 infection: functional and morphological cardiopulmonary changes in elite handball players.

There is increasing evidence of cardiac involvement post-SARS-CoV-2 infections in symptomatic as well as in oligo- and asymptomatic athletes. This study aimed to characterize the possible early effects of SARS-CoV-2 infections on myocardial morphology and cardiopulmonary function in athletes. Eight male elite handball players (27 ± 3.5 y) with past SARS-CoV-2 infection were compared with four uninfected teammates (22 ± 2.6 y). Infected athletes were examined 19 ± 7 days after the first positive PCR test. Echocardiographic assessment of the global longitudinal strain under resting conditions was not significantly changed (- 17.7% vs. - 18.1%). However, magnetic resonance imaging showed minor signs of acute inflammation/oedema in all infected athletes (T2-mapping: + 4.1 ms, p = 0.034) without reaching the Lake-Louis criteria. Spiroergometric analysis showed a significant reduction in VO2max (- 292 ml/min, - 7.0%), oxygen pulse (- 2.4 ml/beat, - 10.4%), and respiratory minute volume (VE) (- 18.9 l/min, - 13.8%) in athletes with a history of SARS-CoV2 infection (p < 0.05, respectively). The parameters were unchanged in the uninfected teammates. SARS-CoV2 infection caused impairment of cardiopulmonary performance during physical effort in elite athletes. It seems reasonable to screen athletes after SARS-CoV2 infection with spiroergometry to identify performance limitations and to guide the return to competition.

Effects of surgical and FFP2/N95 face masks on cardiopulmonary exercise capacity.

BACKGROUND: Due to the SARS-CoV2 pandemic, medical face masks are widely recommended for a large number of individuals and long durations. The effect of wearing a surgical and a FFP2/N95 face mask on cardiopulmonary exercise capacity has not been systematically reported. METHODS: This prospective cross-over study quantitated the effects of wearing no mask (nm), a surgical mask (sm) and a FFP2/N95 mask (ffpm) in 12 healthy males (age 38.1 ± 6.2 years, BMI 24.5 ± 2.0 kg/m2). The 36 tests were performed in randomized order. The cardiopulmonary and metabolic responses were monitored by ergo-spirometry and impedance cardiography. Ten domains of comfort/discomfort of wearing a mask were assessed by questionnaire. RESULTS: The pulmonary function parameters were significantly lower with mask (forced expiratory volume: 5.6 ± 1.0 vs 5.3 ± 0.8 vs 6.1 ± 1.0 l/s with sm, ffpm and nm, respectively; p = 0.001; peak expiratory flow: 8.7 ± 1.4 vs 7.5 ± 1.1 vs 9.7 ± 1.6 l/s; p < 0.001). The maximum power was 269 ± 45, 263 ± 42 and 277 ± 46 W with sm, ffpm and nm, respectively; p = 0.002; the ventilation was significantly reduced with both face masks (131 ± 28 vs 114 ± 23 vs 99 ± 19 l/m; p < 0.001). Peak blood lactate response was reduced with mask. Cardiac output was similar with and without mask. Participants reported consistent and marked discomfort wearing the masks, especially ffpm. CONCLUSION: Ventilation, cardiopulmonary exercise capacity and comfort are reduced by surgical masks and highly impaired by FFP2/N95 face masks in healthy individuals. These data are important for recommendations on wearing face masks at work or during physical exercise.