Objectives The reported prevalence of chronic obstructive pulmonary disease ( COPD ) in people living with HIV ( PLWHIV ) varies widely. Our objective was to estimate the prevalence of airflow obstruction and COPD in unselected PLWHIV and identify characteristics that increase the risk of nonreversible airflow obstruction in order to guide case finding strategies for COPD . Methods All adults attending the Chronic Viral Illness Service were invited to participate in the study, regardless of smoking status or history of known COPD /asthma. Individuals underwent spirometric testing both before and after use of a salbutamol bronchodilator. Airflow obstruction was defined as forced expiratory volume in 1 s ( FEV 1 )/forced vital capacity ( FVC ) < 0.7 post‐bronchodilation, whereas COPD was defined as FEV 1 / FVC < 0.7 post‐bronchodilation and Medical Research Council ( MRC ) score > 2. Multivariate logistic regression was used to evaluate risk factors associated with airflow obstruction, reported as adjusted odds ratios ( aORs ). Results Five hundred and three participants successfully completed spirometry testing. The median (Q1; Q3) age was 52 (44; 58) years. The median (Q1; Q3) CD 4 count was 598 (438; 784) cells/μL and the median (Q1; Q3) nadir CD 4 count was 224 (121; 351) cells/μL. There were 119 (24%) current smokers and 145 (29%) former smokers. Among those screened, 54 (11%) had airflow obstruction whereas three (1%) of the participants had COPD . Factors that were associated with airflow obstruction included a history of smoking [ aOR 2.2; 95% confidence interval ( CI ) 1.1; 4.7], older age (aOR 1.6; 95% CI 1.2; 2.2), and lower CD 4 count (aOR 0.8; 95% CI 0.7; 1.0). Conclusions Airflow obstruction was relatively uncommon. Our findings suggest that PLWHIV who are ≥50 years old, smokers and those with nadir CD 4 counts ≤ 200 cells/μL could be targeted to undergo spirometry to diagnose chronic airflow obstruction.

During the COVID-19 pandemic, there was an urgent need for any medication to help reduce the high death rate experienced during this deadly surge. Remdesivir is an FDA-approved drug for COVID-19 treatment, given its anti-inflammatory properties. Upon extensive literature search, we found two studies and four cases of COVID-19-induced pneumonia treated with remdesivir who were developing bradycardia. In most of these cases, the bradycardia resolved within one-to-two days of holding remdesivir, which correlated with the half-life of remdesivir. Remdesivir was shown to have benefits in COVID-19-induced pneumonia during the COVID-19 surge; however, its use has been controversial. According to the studies, the sinus bradycardia following remdesivir administration does not impact patients’ prognosis in terms of ICU admission and in-hospital mortality. There are multiple case reports noted to report several remdesivir-induced cardiac side effects. In our case, prolonged use and high dosages may induce cardiotoxicity, manifesting as severe bradycardia. Several possible mechanisms for cardiac adverse effects with remdesivir need further investigation and research as COVID-19 remains an active global issue. We present a 53-year-old man hospitalized with COVID-19-induced pneumonia who experienced extreme sinus bradycardia that is likely attributable to remdesivir.

Introduction Low levels of nasal NO have been associated with increased propensity to rhinosinusitis and respiratory tract infections. Our objective was to describe nasal NO levels in HIV-infected individuals versus healthy controls and determine possible risk factors for reduced nasal NO levels. Materials and Methods HIV-infected individuals and healthy controls were recruited. Participants underwent nasal NO testing by standardized methods using a CLD88 chemiluminescence analyzer and completed the Sinonasal Outcome Test-20 (SNOT-20) on symptoms of rhinosinusitis. Results Participants included 41 HIV-infected individuals with suppressed VL on antiretroviral therapy (ART group), 5 HIV-infected individuals with detectable VL off ART (viremic group), and 12 healthy controls (HC group). Mean nasal NO level was 253 (±77) nL/min in the ART group, 213 (±48) nL/min in the viremic group, and 289 (±68) nL/min in the HC group (p = 0.133; ANOVA). There was no correlation between nasal NO level and VL in viremic individuals (r = −0.200; p = 0.747). Differences were observed in mean total points on the SNOT-20 which were 19 (±16)/100, 18 (±26)/100, and 4 (±4)/100 in the ART, viremic, and HC groups, respectively (p = 0.013; ANOVA). Conclusion Healthy individuals, HIV patients on ART, and viremic individuals off ART display similar nasal NO levels. However, rhinosinusitis symptoms remain prominent despite ART-treatment.

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Takotsubo cardiomyopathy (TTC) was initially reported in the 1990s as a reversible cause of cardiomyopathy induced by acute emotional stress. It is characterized by regional systolic dysfunction in the absence of coronary artery disease. We report a case of a 79-year-old woman who was admitted with acute respiratory failure due to pneumonia and was found to have a troponin elevation. Upon further evaluation, the patient was taken to the cardiac catheterization lab and underwent catheterization which showed apical ballooning concerning Takotsubo cardiomyopathy. She was placed on a norepinephrine drip but remained unstable. Milrinone-facilitated diuresis was then initiated with improvement and stabilization in hemodynamics. Takotsubo cardiomyopathy presenting with cardiogenic shock without left ventricular outflow tract obstruction requires treatment with inotropes. Although there is limited data to support the use of milrinone in cardiogenic shock due to TTC, its use in our case facilitated diuresis and improved the patient's outcome after norepinephrine failed to stabilize our patient's hemodynamics. Milrinone inhibits phosphodiesterase type 3 which increases the calcium influx thereby improving the myocardial contraction without any beta agonist action. Therefore, the use of milrinone which is a non-catecholamine inotrope could be considered a better alternative as compared to dobutamine given the underlying pathophysiology of TTC.