Prognostic utility of pulmonary artery and ascending aorta diameters derived from computed tomography in COVID-19 patients.

AIM: Chest computed tomography (CT) imaging plays a diagnostic and prognostic role in Coronavirus disease 2019 (COVID-19) patients. This study aimed to investigate and compare predictive capacity of main pulmonary artery diameter (MPA), ascending aorta diameter (AAo), and MPA-to-AAo ratio to determine in-hospital mortality in COVID-19 patients. MATERIALS AND METHODS: This retrospective study included 255 hospitalized severe or critical COVID-19 patients. MPA was measured at the level of pulmonary artery bifurcation perpendicular to the direction of the vessel through transverse axial images and AAo was measured by using the same CT slice at its maximal diameter. MPA-to-AAo ratio was calculated by division of MPA to AAo. RESULTS: Multivariate logistic regression model yielded MPA ≥29.15 mm (OR: 4.95, 95% CI: 2.01-12.2, p = 0.001), MPA (OR: 1.28, 95% CI: 1.13-1.46, p < 0.001), AAo (OR: .90, 95% CI: .81-.99, p = 0.040), and MPA-to-AAo ratio ≥.82 (OR: 4.67, 95% CI: 1.86-11.7, p = 0.001) as independent predictors of in-hospital mortality. Time-dependent multivariate Cox-proportion regression model demonstrated MPA ≥29.15 mm (HR: 1.96, 95% CI: 1.03-3.90, p = 0.047) and MPA (HR: 1.08, 95% CI: 1.01-1.17, p = 0.048) as independent predictors of in-hospital mortality, whereas AAo and MPA-to-AAo ratio did not reach statistical significance. CONCLUSION: Pulmonary artery enlargement strongly predicts in-hospital mortality in hospitalized COVID-19 patients. MPA, which can be calculated easily from chest CT imaging, can be beneficial in the prognostication of these patients.

Asymmetric dimethylarginine (ADMA) and L-arginine levels in children with glycogen storage disease type I.

Patients with glycogen storage disease type I (GSD-I) often have marked hyperlipidemia with abnormal lipoprotein profiles. This metabolic abnormality improves, but is not fully corrected, with dietary therapy; therefore, these patients may be at high risk for the development of atherosclerosis. A recently discussed cardiovascular risk factor, asymmetric dimethylarginine (ADMA), a naturally occuring product of asymmetric methylation of proteins, is an endogenous inhibitor of endothelial nitric oxide synthase. ADMA causes endothelial dysfunction, vasoconstriction, blood pressure elevation, atherosclerosis, and kidney disease progression. A high prevalence of elevated plasma ADMA levels is observed in adults with hypercholesterolemia, hypertension, chronic kidney disease, diabetes mellitus, peripheral arterial disease, coronary artery disease, preeclampsia, heart failure, liver disease, stroke, and many other clinical disorders. Therefore, we aimed to evaluate the endothelial function in patients with GSD-I by using ADMA levels. High-performance liquid chromatography - based method was used for measuring ADMA and L-arginine levels in plasma. The ADMA level was similar between children with GSD-I and the age-matched healthy control group (0.9±0.28 vs. 1.1±0.45 µmol/L; p=0.18). The L-arginine plasma levels in patients with GSD-I were found to be 55.7±41.3 and 91.6±50.2 µmol/L in healthy controls. The preservation of normal endothelial function may result from diminished platelet aggregation, increased levels of apolipoprotein E, decreased susceptibility of low-density lipoprotein to oxidation (possibly related to the altered lipoprotein fatty acid profile in GSD-I), and increased antioxidative defenses in plasma protecting against lipid peroxidation.

The assessment of atherosclerosis on vascular structures in patients with acute coronary syndrome.

INTRODUCTION: Endothelial dysfunction plays a crucial role in the process of atherosclerotic diseases and has been accepted as an early stage of atherosclerosis. Carotid intima-media-thickness (CIMT) and flow-mediated-dilatation (FMD) of the brachial artery have been recommended as noninvasive methods to assess endothelial structure and function. Angiographic properties of patients with acute coronary syndrome (ACS) are closely associated with cardiovascular events. In this study, we investigated the relation of atherosclerotic properties of coronary, brachial and carotid arteries with CIMT, FMD and coronary angiography in patients with ACS. METHODS: We enrolled 133 patients who were diagnosed with ACS into this study. Exclusion criteria were known coronary artery disease, diabetes mellitus and hypertension. Coronary angiography, CIMT and FMD were measured in all patients. The numbers of major stenotic coronary vessels with > or = 50% or > or = 70% were defined as diseased vessel. Gensini score was used to evaluate the severity of atherosclerosis. Morphologic properties of stenotic lesion were defined. Cutoff levels were 7% for FMD and 0.9 mm for CIMT. RESULTS: Mean age was 59.7 + or - 11.8 years. FMD, CIMT and Gensini score were 8.3 + or - 5.9%, 0.80 + or - 0.19 mm and 7.8 + or - 3.5, respectively. Only 44% of patients with ACS had impaired FMD. Gensini score, number of diseased vessels and number of critical lesions were higher in patients with impaired FMD. (Gensini: 8.7 + or - 3.6 vs. 7.0 + or - 3.1, p = 0.009, diseased vessels: 2.7 + or - 0.4 vs. 2.3 + or - 0.7, p < 0.0001, critical lesions: 3.0 + or - 2.1 vs. 2.2 + or - 1.4, p = 0.02). Increased CIMT was found in only 33% of patients. Gensini score and number of diseased vessels were significantly higher in patients with increased CIMT. Significant but weak correlations were found between CIMT, FMD and angiographic severity of coronary atherosclerosis. Angiographic properties and lesion morphology were similar between CIMT and FMD groups. CONCLUSION: There appears to be a relationship between CIMT, FMD and severity of coronary atherosclerosis in patients with ACS. However, in patients with ACS, morphologic properties of stenotic lesions are not associated with CIMT and FMD in brachial artery.

[Evaluation of adult congenital heart diseases]. / Eriskinlerde görülen dogustan kalp hastaliklarinin degerlendirilmesi.

OBJECTIVES: Data on adult congenital heart diseases (CHD) are limited in Turkey. We evaluated the types and clinical features of CHDs in adult patients followed-up in our center. STUDY DESIGN: This study included 200 adult patients (age >16 years) who were diagnosed as having CHD in our clinic between April 2006 and January 2009. The patients were evaluated in three groups based on the complexity of adult CHD (simple, moderate, or great) according to the most recent ACC/AHA guidelines. RESULTS: There were 121 females (60.5%) and 79 males (39.5%). The mean age was 34.7+/-13.4 years (range 16 to 75 years) and female-to-male ratio was 1.53. The mean age was 32.8+/-14.0 years in males, and 36.0+/-12.9 in females. Nearly half of the patients were in the age groups of 20-29 years (n=46, 23%) and 30-39 years (n=49, 24.5%). According to the ACC/AHA criteria, 145 patients (72.5%) had simple CHD, 34 patients (17%) had moderate CHD, and 21 patients (10.5%) had severe-complex CHD. The mean age tended to decrease as the severity of CHD increased (35.7+/-13.7, 33.2+/-12.4, and 30.5+/-12.2 years, respectively). The most common adult CHD was atrial septal defect (n=105, 52.5%), followed by ventricular septal defect (n=34, 17%), Ebstein's anomaly (n=7, 3.5%), and Eisenmenger's syndrome (n=6, 3%). Aortic coarctation, transposition of the great vessels, patent foramen ovale, pulmonary stenosis, and aortic valve disease showed equal distribution with five patients (2.5%). CONCLUSION: In our study, atrial and ventricular septal defects accounted for the majority of CHDs in adult patients (69.5%). Multicenter studies are required to determine the incidence of CHD among adult population in Turkey.

Does nebivolol prevent contrast-induced nephropathy in humans?

BACKGROUND: An experimental study showed that nebivolol is an effective agent in contrast-induced nephropathy (CIN) prophylaxis. HYPOTHESIS: We hypothesized that prophylactic nebivolol use had protective effects on renal function in human beings subjected to iodinated contrast agent since it has vasodilatory effect and antioxidant properties. METHODS: The present study enrolled 120 patients scheduled for coronary angiography and ventriculography. All patients were hydrated with intravenous isotonic saline. The patients in group I received 600 mg N-acetylcysteine every 12 hours for 4 days. The patients in group II received 5 mg nebivolol every 24 hours for 4 days. The patients in group III were only hydrated. The primary endpoint was the occurrence of CIN. The secondary endpoint was the change in serum creatinine (Cr) levels at 2 days and 5 days after the contrast exposure. RESULTS: Nine (22.5%) patients in group I developed CIN, as did 8 patients (20.0%) in group II and 11 patients (27.5%) in group III (P = 0.72). Changes in mean Cr level from baseline to day 2 were not statistically significant in all groups. However, we detected a statistically significant increase in mean Cr levels at day 5 compared with baseline levels in group I and group III (from 1.42 ± 0.13 to 1.52 ± 0.26, p2 = 0.02; and from 1.43 ± 0.14 to 1.55 ± 0.30, p2 = 0.01, respectively). Although an increase was detected in mean Cr level from baseline to the 5-day Cr level in group II, this did not reach statistical significance (from 1.40 ± 0.12 to 1.48 ± 0.23, P = 0.06). CONCLUSIONS: Pretreatment with nebivolol is protective against nephrotoxic effects of contrast media.

Hemodialysis does not impair ventricular functions over 2 years.

We aimed to evaluate the long-term effect of hemodialysis (HD) treatment on left and right ventricular (LV and RV) functions in patients with end-stage renal disease. The study population consisted of 22 patients with newly diagnosed end-stage renal disease. Before an arteriovenous fistula was surgically created for HD, the patients were evaluated by echocardiography for systolic and diastolic functions. After the first HD session (mean 24.22 ± 2.14 months), the second echocardiographic evaluations were performed. Left ventricular and RV functions before and after long-term HD treatment were compared. The mean age was 55 ± 13 years and 10 (45%) of the patients were female. After long-term HD treatment, the isovolumic relaxation time was significantly decreased; however, the peak early (E) and late (A) diastolic mitral inflow velocities, E/A ratio, and deceleration time of E wave were not significantly different from the baseline measurements. Also, there was no significantly change in the early diastolic velocity (Ea) of the lateral mitral anulus and the E/Ea ratio. Pulmonary vein peak diastolic velocity, peak atrial reversal velocity, and peak atrial reversal velocity duration remained almost unchanged even though the pulmonary vein peak systolic velocity and the pulmonary vein peak systolic velocity/pulmonary vein peak diastolic velocity ratio were significantly lower after long-term HD treatment. In addition, LV systolic functions, LV diameters, LV mass index, left atrium size, and RV diastolic functions were not statistically different after long-term HD treatment. The myocardium is exposed to hemodynamic, metabolic, and neuro-humoral abnormalities during HD treatment; however, the long-term effects of HD on ventricular functions are not clearly known. The present study showed that the long-term effects of HD on LV and RV functions were insignificant in patients with end-stage renal disease. We have demonstrated that the LV and RV functions did not change significantly after long-term HD treatment. We suggest that this result may be due to regulated blood pressure levels of the patients, treatment of anemia and other metabolic disorders during the HD period and the prevention of weight gain and hypervolemia.

Spontaneous coronary artery dissection and pulmonary thromboembolism: a case report.

Spontaneous coronary artery dissection (SCAD) still is a rare cause of acute coronary syndrome. SCAD has been observed in three groups of patients: those with coronary atherosclerosis, peripartal women and idiopathic group. SCAD may be associated with some conditions. We report an unusual association: SCAD and pulmonary thromboembolism.