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Spontaneous coronary artery dissection (SCAD) is an uncommon cause of acute coronary syndrome (ACS) and optimal therapy has not been well-defined. We present a case of long SCAD with complete healing due to medical management. A 47-year-old woman presented to emergency department because of sudden onset of typical chest pain. Electrocardiogram (ECG) showed minimal ST-segment elevation in leads V1–V4. Coronary angiography showed a long spiral dissection extending from the middle segment to the distal segment of the left anterior descending artery and TIMI flow grade three. We decided to follow-up with medical management and have control angiography unless hemodynamic instability and chest pain emerged. Control angiography displayed complete healing of dissect segment after six months. SCAD should be considered, especially in women who present with an ACS without a history of cardiovascular disease and risk factor. This report offers the idea that medical management can be a choice even if in the long segment SCAD setting.

The Brugada Syndrome (BrS) is a heterogeneous genetic disease characterized by persistent or transient ST-segment elevation in the right precordial electrocardiography (ECG) leads and a high incidence of sudden death and life-threatening ventricular tachyarrhythmias in patients with structurally normal hearts. The syndrome generally manifests in men during adulthood. The ECG manifestations can be overt or concealed. We report a case of BrS whose type 1 ECG pattern during febrile state converted to type 2 ECG after alleviation of fever with atypical characteristics (78-year-old woman with monomorphic ventricular tachycardia on holter monitoring, a history of the sudden infant death of her child, and without inducible ventricular arrhythmia by programed ventricular stimulation [PVS]).

Background: Atrial fibrillation (AF) remains the most common arrhythmia following mitral valve surgery. Although numerous clinical and laboratory indicators and possible mechanisms of postoperative AF (PoAF) have been described, the role of microvascular dysfunction in pathogenesis has not been assessed. We aimed to evaluate the association between microvascular dysfunction and PoAF in patients undergoing isolated mitral valve replacement. Methods: 188 patients undergoing mitral valve replacement were included in this retrospective study. Demographic characteristics of the patients were recorded. Angiographic assessment of microvascular perfusion was performed using the myocardial blush grading technique for each patient. Univariate and multivariate logistic regression analyses were utilized to determine predictors of PoAF. Results: Of 188 patients (56.69 ± 8.9 years, 39.4% male) who underwent mitral valve replacement, 64 (34%) patients developed PoAF. In the PoAF group, a lower basal hemoglobin level (12.64 ± 0.89 vs. 14.46 ± 0.91 g/dL; p < 0.001), a higher left atrial diameter [5.9 (5.2–6.47) vs. 4.9 (4.5–5.8) cm; p < 0.001], and a lower total blush score (TBS) (8.33 ± 0.84 vs. 8.9 ± 0.31; p < 0.001) were detected. Multivariate logistic regression analysis revealed that preoperative LA diameter (OR:2.057; 95% CI: 1.166–3.63; p = 0.013), preoperative hemoglobin (OR:0.12; 95% CI: 0.058–0.245; p < 0.001), and abnormal TBS (OR:15.1; 95% CI: 1.602–142.339; p = 0.018) were independent predictors of PoAF. Conclusions: Our findings demonstrated that TBS at the preoperative period was an independent predictor of PoAF in patients undergoing isolated mitral valve replacement.

Objective Atherosclerosis is a chronic, progressive, inflammatory disease. Recognition of subclinical atherosclerotic vascular changes before clinical manifestation in an asymptomatic population is important for risk stratification and optimal management, which finally leads to the prevention of cardiovascular disease. We aimed to determine the risk of premature subclinical atherosclerosis by evaluating epicardial adipose tissue thickness (EATT) and arterial stiffness parameters in patients with ankylosing spondylitis (AS). Methods We performed a prospective study of 60 consecutive patients meeting modified New York criteria for AS compared to 60 controls matched for age and sex. Patients with traditional cardiovascular risk factors were excluded. Arterial stiffness parameters and EATT (examined via echocardiography) values of all patients and control groups were measured. Results There was no difference between basal characteristic and echocardiographic parameters in patients with AS and in the control group. EATT and pulse wave velocity (PWV) were higher in the AS patients compared to the control group. EATT was 5.74 ± 1.22 mm and 4.91 ± 1.21 mm (p

Objective: Endocan, chemerin, and galectin-3 are discrete biomarkers associated with cardiovascular diseases and acting through different pathophysiological pathways. The aim of this study is to investigate and compare the effects of high doses of atorvastatin and rosuvastatin on serum endocan, chemerin, and galectin-3 levels in patients with acute myocardial infarction (AMI). Methods: Sixty-three patients with AMI were randomized to receive atorvastatin (80 mg/day) or rosuvastatin (40 mg/day) after percutaneous revascularization. Serum levels of endocan, chemerin, and galectin-3 were evaluated at baseline and after 4-week therapy. Results: Endocan levels were not decreased statistically significantly with atorvastatin 80 mg, but rosuvastatin 40 mg markedly decreased the levels of endocan according to baseline [from 110.27 (86.03–143.69) pg/mL to 99.22 (78.30–122.87) pg/mL with atorvastatin 80 mg and from 110.73 (77.28–165.22) pg/mL to 93.40 (70.48–115.13) pg/mL with rosuvastatin 40 mg, p=0.242 for atorvastatin 80 mg and p=0.014 for rosuvastatin 40 mg]. Chemerin levels significantly decreased in both groups according to baseline [from 264.90 (196.00–525.95) ng/mL to 135.00 (105.95–225.65) ng/mL with atorvastatin 80 mg and from 309.95 (168.87–701.27) ng/mL to 121.25 (86.60–212.65) ng/mL with rosuvastatin 40 mg, p

A 24-year-old female underwent implantation of a right-sided dual chamber permanent pacemaker for cardioinhibitory syncope with active fixation atrial lead. Five days after the procedure, the patient developed pleuritic chest pain and difficulty in breathing. Minimal pericardial effusion and right hemopneumothorax were found. The atrial active screw-in lead was visualized just above the right atrial appendage with its helix perforating the right atrial wall, pericardium and pleura, reaching the right mid-lobe. Lead extraction was performed, and a passive bipolar atrial lead was implanted during the same session without any problems.