Saara Sillanmäki

Background Obesity is a global issue with a major impact on cardiovascular health. This study explores how obesity influences nocturnal cardiac electrophysiology in suspected obstructive sleep apnea (OSA) patients. Methods We randomly selected 12 patients from each of the five World Health Organization body mass index (BMI) classifications groups ( n total = 60) while keeping the group's age and sex matched. We evaluated 1965 nocturnal electrocardiography (ECG) samples (10 s) using modified lead II recorded during normal saturation conditions. R‐wave peaks were detected and confirmed using dedicated software, with the exclusion of ventricular extrasystoles and artifacts. The duration of waves and intervals was manually marked. The average electric potential graphs were computed for each segment. Thresholds for abnormal ECG waveforms were P‐wave > 120 ms, PQ interval > 200 ms, QRS complex > 120 ms for, and QTc > 440 ms. Results Obesity was significantly ( p < .05) associated with prolonged conduction times. Compared to the normal weight (18.5 ≤ BMI < 25) group, the morbidly obese patients (BMI ≥ 40) had a significantly longer P‐wave duration (101.7 vs. 117.2 ms), PQ interval (175.8 vs. 198.0 ms), QRS interval (89.9 vs. 97.7 ms), and QTc interval (402.8 vs. 421.2 ms). We further examined ECG waveform prolongations related to BMI. Compared to other patient groups, the morbidly obese patients had the highest number of ECG segments with PQ interval (44% of the ECG samples), QRS duration (14%), and QTc duration (20%) above the normal limits. Conclusions Morbid obesity predisposes patients to prolongation of cardiac conduction times. This might increase the risk of arrhythmias, stroke, and even sudden cardiac death.

Background Coronary artery anomalies (CAAs) are congenital disorders associated with variable manifestations and pathophysiological mechanisms. Anomalies can be asymptomatic or cause chest pain, myocardial infarction, or even sudden cardiac death. Case summary We describe a 34-year-old man with a history of a single episode of chest pain. An ectopic origin on the part of the left circumflex (LCX) coronary artery from the proximal right coronary artery (RCA) was evident upon coronary computed tomography angiography. A positron emission tomography perfusion study revealed a stress-induced perfusion defect in the anomalous LCX territory (infero-posterior wall). The patient experienced dyspnoea and ST-segment depression in electrocardiography, suggestive of myocardial ischaemia during the maximal bicycle ergometer stress test. No mechanical compression or stenosis was seen upon invasive coronary angiography. The left ventricular perfusion normalized after the initiation of beta-blocker medication. Discussion Patients with CAAs especially benefit from a multimodality assessment of the vascular territories. In our case, the myocardial perfusion of the infero-posterior wall normalized after treatment with beta-blockers. This may be due to increased coronary vasodilation capacity and myocardial flow reserve, as well as reduced oxygen consumption. Beta-blockers may represent a viable option in low-symptomatic CAA patients with perfusion defect and no ostial stenosis or compression.