Cardiopulmonary Long-Term Sequelae in Patients after Severe COVID-19 Disease.

We aimed to identify cardiopulmonary long-term effects after severe COVID-19 disease as well as predictors of Long-COVID in a prospective registry. A total of 150 consecutive, hospitalized patients (February 2020 and April 2021) were included six months post hospital discharge for a clinical follow-up. Among them, 49% experienced fatigue, 38% exertional dyspnea and 75% fulfilled criteria for Long-COVID. Echocardiography detected reduced global longitudinal strain (GLS) in 11% and diastolic dysfunction in 4%. Magnetic resonance imaging revealed traces of pericardial effusion in 18% and signs of former pericarditis or myocarditis in 4%. Pulmonary function was impaired in 11%. Chest computed tomography identified post-infectious residues in 22%. Whereas fatigue did not correlate with cardiopulmonary abnormalities, exertional dyspnea was associated with impaired pulmonary function (OR 3.6 [95% CI: 1.2-11], p = 0.026), reduced GLS (OR 5.2 [95% CI: 1.6-16.7], p = 0.003) and/or left ventricular diastolic dysfunction (OR 4.2 [95% CI: 1.03-17], p = 0.04). Predictors of Long-COVID included length of in-hospital stay (OR: 1.15 [95% CI: 1.05-1.26], p = 0.004), admission to intensive care unit (OR cannot be computed, p = 0.001) and higher NT-proBNP (OR: 1.5 [95% CI: 1.05-2.14], p = 0.026). Even 6 months after discharge, a majority fulfilled criteria for Long-COVID. While no associations between fatigue and cardiopulmonary abnormalities were found, exertional dyspnea correlated with impaired pulmonary function, reduced GLS and/or diastolic dysfunction.

Systemic Blood Pressure Variation During a 12-Hour Exposure to Normobaric Hypoxia (4500 m).

This study was aimed at evaluating a potential association between blood pressure variation and acute mountain sickness (AMS) during acute exposure to normobaric hypoxia. A total of 77 healthy subjects (43 males, 34 females) were exposed to a simulated altitude of 4500 m for 12 hours. Peripheral oxygen saturation, heart rate, systemic blood pressure, and Lake Louise AMS scores were recorded before and during (30 minutes, 3, 6, 9, and 12 hours) hypoxic exposure. Blood pressure dips were observed at 3-hour mark. However, systolic blood pressure fell more pronounced from baseline during the initial 30 minutes in normobaric hypoxia (-17.5 vs. -11.0 mmHg, p = 0.01) in subjects suffering from AMS (AMS+; n = 56) than in those remaining unaffected from AMS (AMS-; n = 21); values did not differ between groups over the subsequent time course. Our data may suggest a transient autonomic dysfunction resulting in a more pronounced blood pressure drop during initial hypoxic exposure in AMS+ compared with AMS- subjects.