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ObjectiveAlthough numerous studies have shown the protective effects of the well-developed coronary collaterals on left ventricular functions, the relationship between collateral grade and left ventricular end diastolic pressure has not been studied in chronic total occlusion patients. Also, there are conflicting data on the effect of collaterals on NT-proBNP levels. The aim of our study was to evaluate the relationship between coronary collateral circulation and left ventricular end diastolic pressure and NT-proBNP levels in chronic total occlusion patients.MethodsStudy group was retrospectively selected from the patients who had undergone coronary angiography at our hospital between June 2011 and March 2013. Clinical, biochemical, angiographic and hemodynamic data of 199 consecutive patients having at least one totally occluded major epicardial coronary artery were evaluated. Coronary collateral circulation was graded according to Rentrop classification. While Rentrop grade 3 was defined as well-developed, all the remaining collateral grades were regarded as poor collaterals.ResultsOverall 87 patients were found to have good collaterals and 112 patients had poor collaterals. There was no significant difference between the patients with well- or poorly developed coronary collaterals with regard to left ventricular end diastolic pressure (16.84 ± 5.40 mmHg vs 16.10 ± 6.09, respectively, p = 0,632) and log NT-proBNP (2.46 ± 0.58 vs 2.59 ± 0.76, respectively, p = 0,335).ConclusionIn patients with coronary chronic total occlusion even well-developed coronary collaterals are not capable of protecting the rise of left ventricular end diastolic pressure and NT-proBNP levels which are reliable markers of the left ventricular dysfunction.

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The Pulmonary embolism (PE) incidence is higher in patients with chronic kidney disease and renal transplantation (RT) than in general population. Thrombotic events are multifactorial in renal transplantation recipients and hypercoagulability is the most common factor. We present a case of a 67-yearold renal transplant patient with acute, large thrombus in pulmonary arteries and right heart cavities treated successfully with thrombolytic with low dosage in low infusion protocol. Key Words: Pulmonary embolism; Renal transplantation; ThrombolyticA 67-year-old woman was presented with a weeklong chest pain and breathing difficulty. She had a renal transplantation three months ago. She had denied any symptoms after the operation and took drugs-deltacortril 5 mg, prograf 1 mg, certican 0.25 mg, bactrim 400 mg and avalcept 450 mg tb daily. Creatinine level was 1.24 mg/dL and glomerular filtration rate (GFR) was 45. The patient's O 2 was 88% in room atmosphere, breath rate 28 per min, heart rate 120 beat/min, and blood pressure 100/60 mmHg. Laboratory dates was positive: Troponin I (high sensitive) was 0.34 ng/ml, D-dimer was >10.000. Hypoxemia and hypocapnia were seen in Arterial gase analysis: pH 7.31 PaO 2 412, PaCO 2 47, HCO 3 23.3, EB -3.0, SatO 2 99.8%. ECG showed sinus tachycardia with a heart rate of 120 beats/min. Transthoracic echocardiography was performed with a high suspicion of acute pulmonary embolism. TTE showed large, free thrombus moving in right heart cavities. Right heart cavities were dilatated and severe tricuspid regurgitation was revealed with pulmonary artery systolic pressure (sPAB) of 65 mmHg. Pulmonary CT angiography showed an extensive intraluminal and bilateral thrombosis in pulmonary arteries. The diagnosis of acute PE was confirmed. A Doppler ultrasound revealed deep vein thrombosis in right popliteal and crural veins (Figure 1).

Variant angina (VA) is a clinical syndrome caused by spontaneous vasospasm of the epicardial coronary artery which is characterized by episodes of angina. Endothelial dysfunction and neurohormonal hyperactivity are important factors in pathogenesis of VA. Although patient prognosis is good, VA may be one of the reasons of sudden cardiac death (SCD) in case of persistent ST segment elevation and malignant arrhythmias. Therefore, early treatment of VA is crucial for prevention of malignant arrhythmias and SCD. In this case report we describe a case of VA presented with cardiogenic shock and malignant ventricular arrhythmia.