Background: This study aimed to systematically review the evidence of drug-coated balloon used in the treatment of acute myocardial infarction and compared with using drug-eluting stent in terms of clinical and angiographic outcomes for a relatively long follow-up period.

Methods: Electronic databases including PubMed, Embase, and the Cochrane Library were used to search for the information of each study. A total of 8 studies involving 1310 patients were included in this meta-analysis.

Results: During a median follow-up duration of 12 months (range 3-24 months), there were no statistical differences between the drug-coated balloon and drug-eluting stent group in terms of a major adverse cardiovascular event (odds ratio = 1.07; P =.75; 95% CI: 0.72-1.57), all-cause death (odds ratio = 1.01; P =.98; 95% CI = 0.56-1.82), cardiac death (odds ratio = 0.85, P =.65; 95% CI = 0.42-1.72), target lesion revascularization (odds ratio = 1.72; P =.09; 95% CI: 0.93-3.19), recurrent myocardial infarction (odds ratio = 0.89, P =.76; 95% CI: 0.44-1.83), and thrombotic event (odds ratio = 1.10; P =.90; 95% CI: 0.24-5.02). Drug-coated balloon was not linked with risk of late lumen loss compared with drug-eluting stent (mean difference = −0.06 mm; P =.42; 95% CI: −0.22-0.09 mm). However, there was a higher incidence of target vessel revascularization noted in the drug-coated balloon group compared with the drug-eluting stent group (odds ratio = 1.88; P =.02; 95% CI: 1.10-3.22). The subgroup analysis stratified by different study types and ethnicities showed there were no significant differences between the 2 groups.

Conclusions: Using drug-coated balloon might serve as a potential alternative strategy for patients with acute myocardial infarction because of the similar clinical and angiographic outcomes compared with using drug-eluting stent; nevertheless, the issue of target vessel revascularization should be more focused on. Larger and more representative studies are needed in the future.

Background: The risk of cardiovascular disease is correlated with the frequency and control of associated risk factors in diabetes mellitus and may vary according to country. We evaluated risk factors for cardiovascular disease, cardiovascular events, and the use of preventive medications in patients with diabetes mellitus using the Prospective Urban and Rural Epidemiological Türkiye cohort.

Methods: Patients with diabetes mellitus versus without diabetes mellitus were compared for risk factors, cardioprotective drugs (angiotensin-converting enzyme inhibitors or angiotensin-II receptor antagonists, statins, and antiplatelets), and cardiovascular events. The primary outcome was major cardiovascular events (composite of cardiovas-cular death, myocardial infarction, stroke, or heart failure).

Results: Among 4041 participants, 549 (13.6%) had diabetes mellitus. The mean age (54.8 ± 8.4 vs. 49.3 ± 9.0 years, P <.001) and proportion of women (65.4% vs. 59.9%, P =.014) were higher in diabetics compared with non-diabetics. Hypertension, history of coronary heart disease, and use of statin, antiplatelets, and angiotensin-converting enzyme inhibitors or angiotensin-II receptor antagonists were more common in diabetics; however, the use of these medications at baseline was lower than optimal even in patients with diabetes mellitus and concomitant coronary heart disease (statin 31.2%, antiplatelets 46.9%, and angiotensin-converting enzyme inhibitors or angiotensin-II receptor antagonists 54.7%). During 11.5 years of follow-up, major cardiovascular events occurred in 288 (7.1%) patients, and the risk was higher in diabetics [hazard ratio (95% confidence interval) 1.71 (1.30-2.24); P <.001]. The increase in the risk of future events was comparable for those with diabetes mellitus alone without cardiovascular disease [hazard ratio 1.62 (1.20-2.20)] versus those with cardiovascular disease alone without diabetes mellitus [hazard ratio 1.31 (0.83-2.07)] and was additive in those with both conditions [hazard ratio 2.79 (1.65-4.69)]. The risk of major coronary events (myocardial infarction, angina, percutaneous, or surgical coronary intervention) was also higher in diabetes mellitus [hazard ratio 1.64 (1.26-2.15); P <.001].

Conclusion: Patients with diabetes mellitus have a higher risk of major cardiovascular events, and the risk is comparable to that observed in those with cardiovascular disease but no diabetes mellitus. The use of preventive medicines for cardiovascular diseases is disturbingly low in diabetics.

Background: While desmosomal junctions and gap junction remodeling are among the arrhythmogenic substrates, the fate of desmosomal and gap junctions in high-pacing-induced heart failure remains unclear. This aim of this study was to determine the fate of desmosomal junctions in high-pacing-induced heart failure.

Methods: Dogs were randomly divided into 2 equal groups, a high-pacing-induced heart failure model group (heart failure group, n = 6) and a sham operation group (control group, n = 6). Echocardiography and cardiac electrophysiological examination were performed. Cardiac tissue was analyzed by immunofluorescence and transmission electron microscopy. The expression of desmoplakin and desmoglein-2 proteins was detected by western blot.

Results: A significant decrease in ejection fraction, significant cardiac dilatation, diastolic and systolic dysfunction, and ventricular thinning occurred after 4 weeks in high-pacing-induced dog model of heart failure. Effective refractory period action potential duration at 90% repolarization was prolonged in the heart failure group. Immunofluorescence analysis and transmission electron microscopy demonstrated connexin-43 lateralization accompanies desmoglein-2 and desmoplakin remodeling in the heart failure group. Western blotting showed that the expression of desmoplakin and desmoglein-2 proteins was higher in heart failure than in normal tissue.

Conclusion: Desmosome (desmoglein-2 and desmoplakin) redistribution and desmosome (desmoglein-2) overexpression accompanying connexin-43 lateralization were parts of a complex remodeling in high–pacing-induced heart failure.

Background: Systemic immune-inflammatory index (platelet count × neutrophil–lymphocyte ratio) is a new marker that predicts adverse clinical outcomes in coronary artery diseases. Our aim was to investigate the relationship between the systemic immune-inflammatory index and residual SYNTAX score in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention.

Methods: In this retrospective study, 518 consecutive patients who underwent primary percutaneous coronary intervention (PCI) with the diagnosis of ST-segment elevation myocardial infarction were analyzed. The severity of coronary artery diseases was determined by residual SYNTAX score. In the receiver operating characteristic curve analysis, systemic immune-inflammatory index with an optimal threshold value of 1025.1 could detect the presence of a high residual SYNTAX score; the patients were divided into 2 groups as low (326) and high (192) according to the threshold value. In addition, binary multiple logistic regression analysis methods were used to evaluate independent predictors of high residual SYNTAX score.

Results: In binary multiple logistic regression analysis, systemic immune-inflammatory index [odds ratio = 6.910; 95% CI = 4.203-11.360; P <.001] was an independent predictor of high residual SYNTAX score. In addition, there was a positive correlation between the systemic immune-inflammatory index and residual SYNTAX score (r = 0.350, P <.001). In the receiver operating characteristic curve analysis, the systemic immune-inflammatory index with an optimal threshold value of 1025.1 could detect the presence of a high residual SYNTAX score with 73.8% sensitivity and 72.3% specificity.

Conclusion: Systemic immune-inflammatory index, an inexpensive and easily measurable laboratory variable, was an independent predictor of the increased residual SYNTAX score in patients with ST-segment elevation myocardial infarction.

Background: Risk assessment is recommended for patients with congenital heart disease-associated pulmonary arterial hypertension. This study aims to compare an abbreviated version of the risk assessment strategy, noninvasive French model, and an abridged version of the Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management 2.0 risk score calculator, Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management Lite 2.

Methods: We enrolled a mixed prevalent and incident cohort of patients with congenital heart disease-associated pulmonary arterial hypertension (n = 126). Noninvasive French model comprising World Health Organization functional class, 6-minute walk distance, and N-terminal pro-hormone of brain natriuretic peptide or brain natriuretic peptide was used. Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management Lite 2 includes functional class, systolic blood pressure, heart rate, 6-minute walk distance, brain natriuretic peptide/N-terminal pro-hormone of brain natriuretic peptide, and estimated glomerular filtration rate.

Results: The mean age was 32.17 ± 16.3 years. The mean follow-up was 99.41 ± 58.2 months. Thirty-two patients died during follow-up period. Most patients were Eisenmenger syndrome (31%) and simple defects (29.4%). Most patients received monotherapy (76.2%). Most patients were World Health Organization functional class I-II (66.6%). Both models effectively identified risk in our cohort (P =.0001). Patients achieving 2 or 3 noninvasive low-risk criteria or low-risk category by Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management Lite 2 at follow-up had a significantly reduced risk of death. Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management Lite 2 approximates noninvasive French model at discriminating among patients based on c-index. Age, high risk by Registry to Evaluate Early and Long-term Pulmonary Arterial Hypertension Disease Management Lite 2, and the presence of 2 or 3 low-risk criteria by noninvasive French model emerged as an independent predictors of mortality (multivariate hazard ratio: 1.031, 95% CI: 1.005-1.058, P =.02; hazard ratio: 4.258, CI: 1.143-15.860, P =.031; hazard ratio: 0.095, CI: 0.013-0.672, P =.018, respectively).

Conclusions: Both abbreviated risk assessment tools may provide a simplified and robust method of risk assessment for congenital heart disease-associated pulmonary arterial hypertension. Patients not achieving low risk at follow-up may benefit from aggressive use of available therapies.

Background: Atrial fibrillation is a complex disease with irregular ventricular response and tachycardia as a result of irregular and rapid contraction of the atria, with poor cardiovascular outcomes unless treated. Various mechanisms are involved in its pathophysiology..Inflammation has an important place among these mechanisms. Many cardiovascular events accompany inflammation. Understanding and correct evaluation of inflammation in current situations contribute to the diagnosis and severity of the disease. The aim of our study was to understand the role of inflammatory biomarkers in patients with atrial fibrillation and to evaluate the difference between whether the disease is paroxysmal and persistent (atrial fibrillation burden).

Methods: The study was done retrospectively, and a total of 752 patients who were admitted to the cardiology outpatient clinic were recruited. The normal sinus rhythm group of the study consisted of 140 patients, and the atrial fibrillation group consisted of 351 [permanent atrial fibrillation (n = 206) and paroxysmal atrial fibrillation (n = 145)] patients. Inflammation markers were evaluated by dividing the patients into 3 groups.

Results: Higher permanent atrial fibrillation [209.71 (40.73-604.0)], paroxysmal atrial fibrillation [188.51 (53.95-617.46)], normal sinus rhythm [629.47 (104-4695)]; permanent atrial fibrillation [4.53 (0.27-17.94)], paroxysmal atrial fibrillation [3.09 (0.40-11.0)], normal sinus rhythm [2.34 (0.61-13.51)] (P <.05); and permanent atrial fibrillation [1569.54 (139-6069)], paroxysmal atrial fibrillation [1035.09 (133-4013)], normal sinus rhythm [130.40 (26.42-680.39)] (P <.05) were detected in the systemic immune inflammation index, neutrophil–lymphocyte ratio, and platelet/lymphocyte ratio atrial fibrillation groups compared to normal sinus rhythm group. Correlation between C-reactive protein and systemic immune inflammation index (r = 0.679, r = 0.483 P <.05, respectively) was found in the permanent atrial fibrillation and paroxysmal atrial fibrillation groups.

Conclusion: Systemic immune inflammation index, neutrophil–lymphocyte ratio, and platelet–lymphocyte ratio were found to be higher in permanent atrial fibrillation compared to paroxysmal atrial fibrillation and in the whole atrial fibrillation group compared to the normal sinus rhythm group. This indicates that inflammation is associated with AF burden and the SII index is successful in reflecting this.