Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning.

INTRODUCTION: ST segment elevation myocardial infarction (STEMI) due to coronary artery occlusion caused by intracoronary thrombosis in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. We present a case of intracoronary large and mobile thrombus formation after CO poisoning. CASE PRESENTATION: A previously healthy 50-year-old woman was referred for CO poisoning. She had chest pain after exposure to CO. Her initial mental status was preoccupied with chest pain. Her initial CO fraction was 28.1%, and initial laboratory data showed creatine kinase-myocardial isoenzyme of 134 U/L (upper limit 25 U/L) and troponin I of >50 ng/mL (upper limit 0.06 ng/mL). Electrocardiography was carried out on admission, revealing an ST segment elevation in the inferolateral leads. After initial evaluation, coronary angiography was performed and an intracoronary large mobile thrombus was seen in the proximal left anterior descending (LAD) artery with no significant stenosis. We administered tenecteplase with heparin. After the thrombolytic therapy, ST elevation in the inferolateral leads resolved. Repeat angiography was performed after 24 h; the thrombus in LAD had resolved. The patient was discharged after 5 days, with persistent Q wave in the inferior leads and mild hypokinesia of the inferoposterior wall suggesting myocardial injury. CONCLUSION: We describe intracoronary thrombus formation induced by CO poisoning. Because intracoronary thrombus can result in myocardial infarction, its consideration following CO poisoning is important. Patients with CO poisoning who have symptoms of STEMI should be carefully evaluated with serial electrocardiograms, cardiac biomarkers, and an echocardiogram. When there is evidence of acute myocardial injury, a primer in coronary angiography can determine which patients could benefit from intervention.

Increased sympathetic activation in patients with vasovagal syncope is associated with higher mean platelet volume levels.

OBJECTIVES: Vasovagal syncope (VVS) is supposed to be modulated by increased sympathetic tone following an orthostatic maneuver. Increased sympathetic activity may have an important role in mean platelet volume (MPV), either by peripheral activation or by effects on thrombocytopoiesis. We aimed to show the effects of increased sympathetic activity on platelet size in patients with VVS in the present study. PATIENTS AND METHODS: Thirty-seven patients with VVS were compared with age- and sex-matched 33 patients without VVS. All patients have undergone 24 hour holter monitoring for heart rate variability (HRV) and time-domain HRV analysis. Blood samples for MPV measurements were taken before 24 hour holter monitoring. RESULTS: Group 1 was consisted of 37 patients with VVS and group 2 was consisted of 33 patients without VVS. We observed that SDNN, SDNN index, SDSD, RMSDD, PNN50 count were significantly lower and MPV was found significantly higher in patients with VVS (p < 0.05 for all). Pearson's correlation analysis showed that MPV was moderately negatively correlated with SDNN (r = -0.421), SDSD (r = -0.396), NN50 count (r = -0.395) and RMSDD (r = -0.393). Multivariate regression analysis showed that SDNN was the only independent variable, which had a significant effect on increased MPV level (ß = -0.295 , p = 0.016). CONCLUSIONS: We found that MPV was closely associated with increased sympathetic activity in patients with VVS. Our analysis supports the hypothesis that alterations in autonomic status might play a role in the development of platelet size.

Association between microvascular angina and erectile dsyfunction.

Although the origin of cardiac syndrome X (CSX) is still debated, endothelial dysfunction leading to reduced coronary microvascular dilatory response and increased coronary resistance is thought to have an important role in the pathogenesis. Erectile dysfunction (ED) is associated with risk factors resulting in endotelial dysfunction. Although the relationship between cardiovascular disease and ED has been well established; the relation between CSX and ED has not been extensively studied so far. We herein aimed to study ED in patients with CSX. The study was designed as a prospective case-control study. Blood samples were analyzed with respect to concentrations of low-density lipoprotein cholesterol, high-density lipoprotein cholesterol and triglycerides. The subjects answered the native language five-item version of the International Index of Erectile Function Questionnaire (IIEF)-5. Each question was scored from 0 to 5 with a maximum score of 25 denoting healty subjects. We investigated the IIEF-5 score in 51 men with CSX (mean age=48.2±6.4 years), 53 men with demonstrated coronary artery disease (CAD) (mean age=48.3±4.8 years) and 52 male controls with normal coronary arteries (mean age=47.2±6.0 years). Mean IIEF-5 scores were 19.88±3.07 for CSX group, 18.83±3.31 for CAD group and 21.40±2.94 for control group. IIEF-5 scores in CSX group were found to be significantly lower than the those of control group (P<0.001). There were no significant differences in IIEF-5 scores between CSX and CAD groups (P=0.09). We have shown for the first time that patients with CSX have lower IIEF-5 scores compared with controls with normal coronary angiograms. This study suggests that ED and CSX may be different manifestations of a common underlying vascular pathology and vasculogenic ED is frequently seen in CSX at least as much as in CAD.

Percutaneous closure of a tricuspid paravalvular leak with an Amplatzer duct occluder II via antegrade approach.

Paravalvular leaks are seen after valve-replacement surgery and most patients with these leaks are asymptomatic, probably due to the small size of the leak. Nevertheless, a paravalvular leak after tricuspid valve replacement is a rare complication and may cause severe haemoylsis and hepatic dysfunction. It is usually treated surgically. There are no data on percutaneous transcatheter closure of paravalvular leaks. In this report, we present a successful percutaneous closure of a paravalvular leak using an Amplatzer duct occluder II device after a tricuspid valve replacement in a patient with high operative risk who had also had mitral and aortic valve replacements.

A coronary artery anomaly: type IV dual left anterior descending artery.

Coronary artery anomalies are seen in about 1.3% of patients undergoing coronary angiography. However, the dual type of left anterior descending (LAD) artery is a rare form of coronary artery anomaly. There are four types of dual LAD; type IV describes the anomaly of a rudimentary LAD artery terminating in the mid-portion of the anterior interventricular sulcus, and the presence of another LAD originating from the right coronary artery and continuing to the anterior interventricular sulcus.

An unusual case of an obtuse marginal branch supplying the left ventricular apex.

In most patients, the left anterior descending coronary artery (LAD) feeds the anterior aspect of the interventricular septum and a large segment of the anterior wall of the left ventricle. It then passes around the left ventricular apex to supply that area as well. However, in some cases, the LAD is shorter and terminates either at or before the left ventricular apex. The latter in these cases is instead supplied by a long posterior descending coronary artery (PDA), originating from the right coronary artery (RCA) at the crux, then passing along the entire length of the posterior interventricular groove, and either terminating at the apex or extending beyond it to pass upward in the anterior interventricular groove. In this case report, we describe a 50-year-old man with an apical perfusion defect on stress myocardial perfusion imaging in whom diagnostic coronary angiography revealed that the left ventricular apex was supplied by a large, obtuse marginal branch of the left circumflex coronary artery (LCX) instead of the LAD.

Bilateral coronary-pulmonary artery fistulae associated with severe aortic insufficiency: an interesting association causing myocardial ischemia.

BACKGROUND: Coronary artery fistula (CAF) is defined as a direct communication of a coronary artery with a cardiac chamber, great vessel or other vascular structure, bypassing the myocardial capillary bed. Congenital CAFs joining into the pulmonary artery are rare cardiac anomalies. CAFs arising from two coronary arteries are even more rare especially when combined with valvular heart disease. The coincidence of CAFs with aortic insufficiency is relatively rare and sometimes might cause myocardial ischemia. RESULTS: We present a case of bilateral coronary-pulmonary artery fistula combined with severe aortic insufficiency causing myocardial ischemia and who subsequently underwent fistula ligation during aortic valve surgery.

Spironolactone does not prevent restenosis after coronary stenting in humans.

INTRODUCTION: In animal studies, aldosterone enhanced neointimal proliferation by increasing extracellular accumulation of collagen and potentiating the effects of angiotensin II. Spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal proliferation. We conducted a placebo-controlled, double-blind, randomised study to assess the effect of spironolactone on angiographic 6-month in-stent restenosis. MATERIALS AND METHODS: Of the 310 randomised patients with significant coronary artery disease, 258 patients were available for analysis: 128 constituted the placebo group and 130 were assigned to receive spironolactone. Eligible patients were randomly assigned to receive a dose of 50 mg spironolactone or placebo orally twice a day for 6 months. The primary endpoint was the angiographic restenosis (>50% stenosis) rate at follow-up angiography. RESULTS: At 6-month follow-up angiography after stenting, there was no difference between the 2 groups in minimal lumen diameter, percent diameter stenosis, late loss, and net gain. Angiographic restenosis occurred in 46 (35.4%) of 130 patients receiving spironolactone and 50 (39.0%) of 128 in the placebo group with an odds ratio (OR) of 0.85 with a 95% confidence interval (CI) of 0.49 to 1.46 (P = 0.62). Restenosis rate was found in 60 (32.9%) of 182 lesions in the spironolactone group, and 61 (35.5%) of 172 lesions in the placebo group with an OR of 0.89 with a 95% CI of 0.56 to 1.42 (P = 0.89). CONCLUSIONS: Spironolactone did not reduce the incidence of in-stent restenosis as compared with placebo in human, contrary to the fact that reduction of neointimal formation in animal models has been observed upon administration of spironolactone.

Lumen loss in transplant coronary artery disease is a biphasic process involving early intimal thickening and late constrictive remodeling: results from a 5-year serial intravascular ultrasound study.

BACKGROUND: Coronary artery disease is the major cause of late cardiac allograft failure. However, few data exist regarding the natural history of changes in intimal and external elastic membrane (EEM) areas after heart transplantation. METHODS AND RESULTS: In 38 transplant recipients, serial intravascular ultrasound examinations were performed 3.7+/-2.2 weeks after transplantation and annually thereafter for 5 years. In 59 coronary arteries, we compared 135 matched segments among serial studies. In each segment, intravascular ultrasound images were digitized at 1-mm intervals, and mean values of EEM and lumen and intimal areas were analyzed. In the first year after transplantation, the intimal area increased significantly from 1.8+/-1.6 to 3.0+/-2.1 mm(2) (P<0.001). Subsequently, the annual increase in intimal area decreased. EEM area did not change during the first year; however, between years 1 and 3, significant expansion of EEM area occurred (15.4+/-4.6 to 17.2+/-5.4 mm(2), P<0.001). Thereafter, EEM area decreased significantly from 17.2+/-5.4 mm(2) (year 3) to 15.1+/-4.9 mm(2) (year 5, P=0.01). Different mechanisms of lumen loss were observed during 2 phases after transplantation: early lumen loss primarily caused by intimal thickening and late lumen loss caused by EEM area constriction. CONCLUSIONS: This serial ultrasound study revealed that most of the intimal thickening occurred during the first year after heart transplantation. Changes in the EEM area showed a biphasic response, consisting of early expansion and late constriction. Thus, different mechanisms of lumen loss were observed during the early and late phases after transplantation.