Hossein Sheibani

Background: The coronary slow flow phenomenon (CSFP) is an angiographic finding attributed to coronary microvascular dysfunction. Given the overlap in cardiovascular manifestations between COVID‐19 and CSFP, the potential association of COVID‐19 with the proportion and angiographic severity of CSFP remains poorly understood. Methods: This retrospective cross‐sectional study included 242 eligible patients with angiographically diagnosed CSFP at Imam Hossein Hospital, Shahroud, Iran, from April 2018 to April 2023. The primary analysis compared the proportion of CSFP among all coronary angiography procedures before and during the COVID‐19 pandemic. Secondary analyses compared clinical characteristics and laboratory parameters according to COVID‐19 status and angiographic CSFP severity. Results: During the COVID‐19 pandemic, the proportion of angiographically diagnosed CSFP among patients undergoing coronary angiography increased significantly compared with the prepandemic period (8.0% vs. 3.5%, p < 0.01). However, angiographic CSFP severity did not differ before and during the pandemic ( p = 0.58). Among the 242 eligible patients, 88 (36.4%) had documented COVID‐19. Overall, 113 patients (46.7%) had mild CSFP and 129 patients (53.3%) had severe CSFP. Multivariable logistic regression, adjusted for age, sex, and underlying disease, showed that non‐COVID‐19 patients had higher odds of severe CSFP than COVID‐19 patients (OR = 1.73; 95% CI, 1.013, 2.960). Conclusion: This study provides novel evidence regarding changes in the proportion and angiographic severity of CSFP before and during the COVID‐19 pandemic. The findings suggest that the observed differences may reflect changes in clinical presentation, referral patterns, or diagnostic evaluation during the pandemic rather than evidence of a causal relationship between COVID‐19 and CSFP pathophysiology. Further prospective studies with precise exposure timing and functional assessment of coronary microvascular function are required to better clarify the relationship between COVID‐19 and CSFP pathophysiology and the mechanisms underlying these observations.

Introduction In late 2019, the first case of a patient with pneumonia of unknown cause was reported in Wuhan, China. The disease, called coronavirus disease 2019 (COVID-19), spread rapidly and caused a pandemic. The virus that causes this infection is called severe acute respiratory syndrome coronavirus 2 (SARS-CoV ...

Introduction: Coronavirus-2019 (COVID-19) spreads rapidly worldwide and causes severe acute respiratory syndrome. The current study aims to evaluate the relationship between the whole-brain functional connections in a resting state and cognitive impairments in patients with COVID-19 compared to the healthy control group. Methods: Resting-state functional magnetic resonance imaging (rs-fMRI) and Montreal cognitive assessment (MoCA) data were obtained from 29 patients of the acute stage of COVID-19 on the third day of admission and 20 healthy controls. Cross-correlation of the mean resting-state signals was determined in the voxels of 23 independent components (IC) of brain neural circuits. To assess cognitive function and neuropsychological status, MoCA was performed on all participants. The relationship between rs-fMRI information, neuropsychological status, and paraclinical data was analyzed. Results: The COVID-19 group got a lower mean MoCA score and showed a significant reduction in the functional connectivity of the IC14 (P<0.001) and IC38 (P<0.001) regions compared to the controls. The increase in functional connectivity was observed in the COVID-19 group compared to the controls at baseline in the default mode network (DMN) IC00 (P<0.001) and dorsal attention network (DAN) IC08 (P<0.001) regions. Furthermore, the alternation of functional connectivity in the mentioned ICs was significantly correlated with the mean MoCA scores and inflammatory parameters, i.e. erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). Conclusion: Functional connectivity abnormalities in four brain neural circuits are associated with cognitive impairment and increased inflammatory markers in patients with COVID-19.

Background: Rapid diagnosis of coronary artery disease has an important role in saving patients. The aim of this study is to evaluate if aVR lead ST-elevation (STE) can predict LM/3VD, left main (LM) disease, and three-vessel disease (3VD), outcome in acute coronary syndrome (ACS) patients. Methods: In this systematic review and meta-analysis, 45 qualified studies were entered. Scopus, Pub med, Google scholar, Web of science, Cochrane library were searched on 12 November 2021. Results: This systematic review includes 52,175 participants. In patients with STE, the total odds ratios for LM, 3VD, and LM/3VD were 5.48 (95% CI 3.88, 7.76), 2.21 (95% CI 1.78, 3.27), and 6.21 (95% CI 3.49, 11,6), respectively. STE in lead aVR was linked with in-hospital death (OR = 2.99, CI 1.90, 4.72) and 90-day mortality (OR = 3.09, CI 2.17, 4.39), despite the fact that it could not predict 30-day mortality (OR = 1.11, CI 0.95, 1.31). The STE > 1 mm subgroup had the highest sensitivity for LM (0.9, 95% CI 0.82, 0.98), whereas the STE > 0.5 mm (0.76, 95% CI 0.61, 0.90) subgroup had the highest sensitivity for LM/3VD. The appropriate cut-off point with highest specificity for LM/3VD and LM was STE > 1.5 mm (0.80, 95% CI 0.75, 0.85) and STE > 0.5 mm, respectively (0.75, 95% CI 0.67, 0.84, I² = 97%). Conclusion: The odds of LM and LM/3VD were higher than 3VD in ACS patients with STE in lead aVR. Also, STE > 0.5 mm was the best cut-off point to screen LM/3VD, whereas for LM diagnosis, STE > 1 mm had the highest sensitivity. Furthermore, LM/3VD had a higher overall specificity than LM.

Background: Serum vitamin D levels may have a protective role against severe coronavirus disease 2019 (COVID-19). Studies have shown that deficiency in vitamin D may be a significant risk factor for poor outcomes. This study aims to compare the outcome and clinical condition of patients diagnosed with COVID-19 infection considering serum vitamin D levels.Methods: In this cross-sectional study, 202 COVID-19 patients without known cardiovascular disease (reduced ejection fraction, uncontrolled arrhythmia, pericardial effusion, cardiac block, valvular disease, or hypertension) were included. Patients were divided into three groups of insufficient (< 30 ng/mL), normal (30 to 50 ng/mL), and high (> 50 ng/mL) serum vitamin D levels. Clinical outcome was defined as severe if invasive respiratory intervention and ICU admission was required.Results: The patients were divided into three groups based on their vitamin D level: 127 cases in the insufficient vitamin D group, 53 cases in the normal vitamin D group, and 22 cases in the high vitamin D group. The mean age of the population study was 56 years. Thirty-four patients had severe clinical outcomes. The distribution of this group was as follows: 21 patients in the insufficient vitamin D group (16.5%), eight patients in the normal vitamin D group (15.1%), and five patients in the high vitamin D group (22.7%); P = 0.74. No significant differences were found between the groups in terms of mortality rate (P = 0.46). Moreover, the mean of leukocytes (mean ± SD = 6873.5 ± 4236.2), ESR (mean ± SD = 38.42 ± 26.7), and CPK-MB (mean ± SD = 63 ± 140.7) were higher in the insufficient vitamin D group, but it was not statistically significant (P > 0.05).Conclusion: The finding of the present study showed that vitamin D could not make a significant difference in cardiovascular systems, laboratory results, and severity of the disease in COVID-19 patients.

This study is about an infrequent first presentation of Aortic Dissection (AD), and it is primary Ventricular Fibrillation (VF). We present a 64-year-old woman with a history of hypertension who came with sudden retrosternal chest pain, dizziness, nausea, and vomiting. The patient suffered a cardiac arrest a few seconds after admission. Cardiopulmonary resuscitation (CPR) was done for her. An electrocardiogram (ECG) showed ST elevation that demonstrated acute anterior MI (Myocardial Infarction). Trans-thoracic echocardiography (echo) CT angiography demonstrated decreased left ventricular ejection fraction with normal LV size (LVEF=25%) and type A Stanford and type I DeBakey aortic dissection flap from root up to distal of abdominal Aorta. This is while the patient's first presentation was VF, and she had anterior MI, which is unusual for aortic dissection. Therefore, we must consider AD in patients with VF. We have to consider AD in anterior MI patients because of the contraindication of medication.

Background: The prevalence of cardiovascular complications in COVID-19 infection varied in different studies. One of these complications is myocardial infarction. A disturbance of the blood supply can lead to myocardial infarction by clot formation in the arteries. However, no evidence of significant coronary stenosis has been found in more than 50% of patients with COVID-19 and ST elevation.Case Presentation: 38 and 49 years old men (patients 1,2) were admitted to our hospital with the complaint of typical chest pain and COVID-19 symptoms. The real-Time Polymerase Chain Reaction (RT-PCR) test confirmed COVID-19 in both. Patient 1 represented inferior posterior ST-Elevation Myocardial Infarction (STEMI) in his electrocardiogram (ECG). Also, patient 2 has ST-elevation in high lateral and septal leads (I, AVL, V1, V2) and ST-segment depression in AVR and inferior leads (III, AVF). Their troponin was positive. The vital signs were normal in both of them. Patient 2 just had a history of aortic valve replacement (AVR) 5 years ago. However, Patient 1 had no medical history. Transthoracic Echocardiography (TTE) data demonstrated some disturbances in patient 1 Severe hypokinesia of Inferior, Posterior, Lateral, and Septal walls. However, TTE data were unremarkable for patient 2. We prescribed recommended medications for them. Therefore, their ECG changes were corrected, and his condition improved. In addition, Coronary angiography was done that demonstrated patent and normal coronary arteries in both of them.Conclusion: COVID-19 infection can cause normal coronary arteries myocardial infarction with probable two mechanisms prolonged vasospasm or intraluminal coronary thrombogenesis.

Prinzmetal angina is one of the causes of acute coronary syndromes, the exact etiology of which is still unknown. Here we introduce a 27-year-old man with no history of cardiovascular disease, with a history of hospitalization due to acute pericarditis in the previous month, who was discharged with a good response to ibuprofen treatment but had clinical and electrocardiographically recurrence of pericarditis with compressive retrosternal chest pain and electrocardiogram (ECG) changes in favor of acute infero-postero-right ventricular (RV) myocardial infarction (MI). Treatment with vasodilator improved compressive retrosternal chest pain and reversed acute myocardial infarction changes completely and left pleuritic chest pain and pericarditis changes in the ECG. Due to the typical chest pain, he was admitted to the emergency room; ECG revealed generalized ST-segment elevation with acute pericarditis pattern again. Acute infero-posterior and right ventricular acute myocardial infarction pattern was also evident. After treatment with nitroglycerin in the Critical Cardiac Unit (CCU), all ECG ischemic changes returned to baseline, and pericarditis remained in all leads. The patient was discharged with non-steroidal anti-inflammatory drugs (NSAIDs), calcium channel blockers, and a good general condition.