Increased endothelin-1 levels in coronary artery disease with diabetes mellitus in an Indonesian population.

Diabetes mellitus (DM) increases risk of coronary artery disease (CAD). Endothelin-1 (ET-1) is a potential biomarker of endothelial dysfunction. This study aimed to evaluate ET-1 level in CAD patients and its relationship with DM. The cross-sectional design included subjects with angiographically proven CAD and controls among Indonesian. DM was defined by medical history and anti-diabetics use. Serum ET-1 level was measured in both subject groups. We recruited 305 subjects, 183 CAD patients and 122 controls. CAD subjects had higher percentage of males, DM, hypertension, dyslipidemia, smoking, family history of cardiovascular disease, and obesity. ET-1 level was significantly higher in CAD than in controls (2.44 ± 1.49 pg/mL vs. 1.76 ± 0.83 pg/mL; p < 0.001). Increased ET-1 level was significantly associated with DM and dyslipidemia. The highest ET-1 level was observed in CAD with DM, followed by CAD non-DM (2.79 ± 1.63 pg/mL vs. 2.29 ± 1.40 pg/mL; p = 0.023). Among controls, ET-1 level was the lowest in non-DM subjects. Female CAD had higher proportion of DM; however, ET-1 level was similar to male CAD with DM. In conclusion, an increased ET-1 level was significantly associated with DM in patients with CAD. Further research should investigate the potential role of ET-1 receptor antagonists in the secondary prevention of CAD with DM.

Possible silent hypoxemia in a COVID-19 patient: A case report.

INTRODUCTION: It has been hypothesized that silent hypoxemia is the cause of rapid progressive respiratory failure with severe hypoxia that occurs in some COVID-19 patients without warning. PRESENTATION OF CASE: A 60-year-old male presented cough without any breathing difficulty. Vital signs showed blood pressure 130/75 mmHg, pulse 84x/minute, respiratory rate (RR) 21x/minute, body temperature 36.5C, and oxygen saturation (SpO2) 75% on room air. RT-PCR for COVID-19 were positive. On third day, he complained of worsening of breath shortness, but his RR was still normal (22x/minute) with SpO2 of 98% on 3 L/minute oxygen via nasal cannula. On fifth day, he experienced severe shortness of breath with RR 38x/minute. He was then intubated using a synchronized intermittent mandatory ventilation. Blood gas analysis showed pH 7.54, PaO2 58.9 mmHg, PaCO2 31.1 mmHg, HCO3 26.9mEq/L, SaO2 94.7%, FiO2 30%, and P/F ratio 196 mmHg. On eighth day, his condition deteriorated with blood pressure 80/40 mmHg with norepinephrine support, pulse 109x/minute, and SpO2 72% with ventilator. He experienced cardiac arrest and underwent basic life support, then resumed strained breathing with return of spontaneous circulation. Blood gas analysis showed pH 7.07, PaO2 58.1 mmHg, PaCO2 108.9 mmHg, HCO3 32.1mEq/L, SaO2 78.7%, FiO2 90%, and P/F ratio 65 mmHg. Three hours later, he suffered cardiac arrest again and eventually died. DISCUSSION: Possible mechanisms of silent hypoxemia are V/Q mismatch, intrapulmonary shunting, and intravascular microthrombi. CONCLUSIONS: Silent hypoxemia might be considered as an early sign of deterioration of COVID-19 patients, thus, physician may be able to intervene early and decrease its morbidity and mortality.