Maryam Nabati

Troponin-I elevation during a COVID-19 infection is likely due to multiple factors. Few studies have investigated the relationship between troponin levels and echocardiographic variables in patients with COVID-19. Our study aimed to evaluate the clinical and paraclinical effects—including echocardiographic findings—of COVID-19 on myocardial injury, as indicated by elevated troponin levels, and to assess its potential impact on in-hospital and three-month outcomes in hospitalized COVID-19 patients. In this historical cohort study conducted at the Heart Hospital between 2021 and 2022, 161 hospitalized patients were included—72 with elevated troponin and 89 with normal troponin levels. Daily blood tests assessed complete blood count, electrolytes, blood sugar, CRP, blood urea nitrogen (BUN), and creatinine. All patients underwent transthoracic echocardiography within 24 h of admission to evaluate cardiac parameters, including left atrial and ventricular diameters, left ventricular (LV) ejection fraction, right ventricular (RV) size and function, and pulmonary artery pressure. The troponin-positive group had a significantly higher prevalence of a history of cardiovascular disease compared to the troponin-negative group (65.3% vs. 40.4%, P = 0.01). Also, blood sugar, white blood cell count, BUN, and creatinine levels were significantly higher in the troponin-positive group (P = 0.035, 0.006, 0.006, and 0.006, respectively). Echocardiographic findings showed a significantly higher prevalence of left ventricular (LV) enlargement, LV systolic dysfunction, right ventricular (RV) systolic dysfunction, pulmonary hypertension, and significant mitral regurgitation in the troponin-positive group (P = 0.006 for all). Three- month mortality [9(23.1%) vs. 4(5.8%), P value = 0.048] was higher in in troponin-positive group than troponin negative group. Moreover, patients in troponin positive group had 6.6 times higher odds of death (OR = 6.64, 95% CI: 1.28–34.37, p = 0.024). The results of our study suggest that elevated troponin levels in COVID-19 patients may serve as a marker of increased risk for more severe disease, significant left and right ventricular dysfunction, pulmonary hypertension, and higher mortality compared to those without elevated troponin levels. Clinical trial number: Not applicable.

Periodontitis is a chronic inflammatory disease of the supporting tissue surrounding the teeth. The disease is caused by specific bacteria, such as Porphyromonas gingivalis, which lead to the destruction of periodontal ligaments and alveolar bone. The study aimed to evaluate the relationship between the prevalence of P. gingivalis in subgingival plaque and coronary artery disease (CAD). Fifty patients with CAD and 50 healthy controls (non-CAD) participated in this case-control study. The periodontal health in the groups was evaluated through the assessment of the pocket depth (PD), clinical attachment loss (CAL) and bleeding on probing (BoP). The presence of P. gingivalis in subgingival plaque samples was determined through real-time polymerase chain reaction (RT-PCR). The data was analyzed using the χ2 test and the Mann-Whitney U test. The mean PD was 3.30 ±1.55 mm and 3.56 ±0.97 mm in CAD patients and non-CAD subjects, respectively (p = 0.028). No significant differences were observed in the CAL (p = 0.858) and BoP (p = 1.000) between the groups. The RT-PCR results revealed the presence of P. gingivalis 16S rDNA in 32% and 22% of the subgingival plaque of patients with CAD and non-CAD, respectively, with a mean concentration of 7.7 × 106. No statistically significant association was observed between the prevalence of P. gingivalis and CAD (p = 0.260). The results of the multiple logistic regression analysis showed an association between CAD and male sex (p = 0.004, odds ratio (OR): 4.163), as well as age (p = 0.011, OR: 1.067). The findings of this study indicated that there is no statistically significant correlation between the prevalence of P. gingivalis in subgingival plaque and CAD.

There is little information about the risk of drug-induced QT prolongation by remdesivir as the most important FDA approved anti COVID-19 drug. Prolongation of corrected QT interval (QTc) is considered as an indicator of an unfavorable outcome which may ultimately induce torsade de pointes and provoke ventricular fibrillation. The aim of this study was to determine the effects of remdesivir on QTc in patients with severe COVID 19 disease. A historical cohort study was conducted on 249 patients who experienced severe COVID-19 disease and were candidate for treatment by intravenous remdesivir. We obtained a 12 lead electrocardiogram at the admission time and five days later to find any significant change in QTc and QT interval following therapy. We took blood samples at the time of hospitalization and then every day to determine the serum levels of electrolytes, complete blood count, fasting blood sugar (FBS), creatinine (Cr), and complete blood count. The results of this analysis showed blood pressure and heart rate (HR) were lower and total white blood cells and neutrophil counts, FBS and Cr levels were higher at fifth day than first day of study (P value < 0.001). Furthermore, QT interval was more prolonged at fifth day compared with beginning of remdesivir therapy (379.51 ± 34.90ms vs. 366.72 ± 30.97ms, P value < 0.001). However, QTc was not significantly increased at fifth day in comparison with first day (402.37 ± 33.62ms vs. 400.76 ± 30.18ms, P value = 0.524 by Bazett’s formula and 402.81 ± 36.33 vs. 400.78 ± 32.49, P value = 0.459 by Fridericia’s formula). The current study found no evidence linking the administration of remdesivir with prolongation of the QTc interval.

Background Non-ST-segment elevation myocardial infarction (NSTEMI) is more common than ST-segment elevation myocardial infarction (STEMI), consisting of 60–70% of myocardial infarctions. When left ventricular (LV) pressure increases during early systole, regionally ischaemic myocardium with a reduced active force exhibit stretching. The aim of this study was to evaluate the role of this parameter in determining high risk angiographic territory involvement in NSTEMI patients. Results This study was a descriptive correlational research that was conducted on 96 patients with NSTEMI and a left ventricular ejection fraction ≥ 50% who underwent coronary angiography (CAG). Patients were divided into two groups based on having or not having high risk angiographic territory involvement in CAG. All patients underwent a transthoracic echocardiography during the first day of hospitalization and early systolic lengthening (ESL), duration of ESL (DESL), left ventricular global longitudinal strain (LVGLS), pulsed-wave Doppler-derived transmitral early (E wave) and late (A wave) diastolic velocities, and tissue-Doppler-derived mitral annular early diastolic (e′) and peak systolic (s′) velocities were determined. The results of this study showed DESL, DESL_LAD, and DESL_LCX were longer in high risk angiographic territory group than other one (P value 0.016, 0.044, and 0.04, respectively). The logistic regression analysis showed among different variables, only age and ESL_LAD had an independent association with high risk angiographic territory involvement (P = 0.01, odds ratio [OR] 1.09, 95% CI 1.021–1.164, and P = 0.024, odds ratio [OR] 1.243, 95% CI 1.029–1.50, respectively). Conclusions Assessment of myocardial ESL_LAD by speckle-tracking echocardiography may be helpful in predicting high risk angiographic territory involvement in patients with NSTEMI. Indeed, a higher value can be considered as a high risk parameter which may show benefit of an early invasive strategy versus a conservative approach.

The present study aimed to respond to clinical question, can prolonged P-R interval predict clinical outcomes in non-ST elevation acute coronary syndrome patients? This descriptive-analytical study was conducted on cardiac patients. All of the non-ST elevation acute coronary syndrome (NSTEACS) including non-ST elevation myocardial infarction (NSTEMI) and unstable angina patients included in the study. Then they divided into two groups: prolonged P-R interval and normal P-R interval. The patients who had a history of digoxin and calcium channel blocker use, using antiarrhythmic drugs, known valvular or congenital heart disease and connective tissue, unreadable P-R interval and cardiac block were excluded. Data were collected using the questionnaire consisted demographic data and clinical outcomes and a follow-up part was completed by one of the researchers. Finally, 248 patients completed the study. The results showed both of the two groups had significant differences in terms of the history of myocardial infarction (MI) (p = 0.018), the level of high-density lipoprotein (HDL) (p = 0.004), heart rate (p = 0.042), inverted T wave (p = 0.017), anterior ST- segment depression (p = 0.008), normal report of coronary angiography (CAG) (p = 0.003), three vessels disease (p = 0.043), left main lesion (p = 0.045) and SYNTAX score (p = 0.032) based on the CAG report. The results of six-month follow-up showed although, the frequency of ischemic stroke, coronary artery disease (CAD) and cardiovascular death were higher in prolonged P-R interval groups. The chi-square test showed this difference was statistically non-significant (p > 0.05). The multivariate logistic regression model revealed non-significant relationships between prolonged P-R interval and SYNTAX score, significant CAD, three-vessel disease, inverted T wave, anterior ST depression, heart rate and HDL. Based on the results of our study the six-month follow-up showed non-significant outcomes. Further studies are recommended to assess the long-term outcomes.

Background: Diabetes mellitus (DM) has been documented among the strongest risk factors for developing heart failure with preserved ejection fraction (HFpEF). The earliest imaging changes in patients with DM are the left atrial (LA) functional and volumetric changes. The aim of this study was to determine the correlation between epicardial fat thickness (EFT) and longitudinal LA reservoir strain (LARS) in patients with type 2 DM (T2DM), as compared with non-diabetic controls. Results: The study samples in this case-control study comprised of consecutive patients with T2DM (n=64) and matched non-diabetic controls (n=30). An echocardiography was performed on all patients and EFT, volumetric and longitudinal LARS, left ventricular (LV) global longitudinal strain (LVGLS), pulsed-wave Doppler-derived transmitral early (E wave) and late (A wave) diastolic velocities, and tissue-Doppler-derived mitral annular early diastolic (e′) and peak systolic (s') velocities were obtained. The study results demonstrated that the patients with T2DM had thicker EFT (5.96±2.13 vs. 4.10±3.11 mm) and increased LA volume index (LAVI) (43.05± 44.40 vs. 29.10±11.34 ml/m ² ) in comparison with the non-diabetic ones (p-value: 0.005 and 0.022, respectively). On the other hand, a direct association was observed between EFT and the E/e′ ratio, and an inverse correlation was established between EFT and LARS in patients with T2DM (r=0.299, p-value=0.020 and r=− 0.256, p-value=0.043, respectively). However, regression analysis showed only LV mass index (LVMI) (β=0.012, 95% CI 0.006–0.019, p-value<0.001), LAVI (β=− 0.034, 95% CI − 0.05–0.017, p-value<0.001), and EFT (β=− 0.143, 95% CI − 0.264–− 0.021, p-value=0.021) were independently correlated with LARS. Conclusions: LARS is considered as an important early marker of subclinical cardiac dysfunction. Thickened epicardial fat may be an independent risk factor for decreased LA reservoir strain. Diabetics are especially considered as a high risk group due to having an increased epicardial adipose tissue thickness.