25 hydroxyvitamin D levels in patients undergoing coronary artery catheterization.

INTRODUCTION: A growing body of evidence suggests that vitamin D deficiency is associated with increased cardiovascular morbidity and mortality. The present study assessed the association between low serum 25-hydroxyvitamin D (25(OH)D) and coronary artery disease status defined by coronary catheterization findings. METHODS: An observational study of 101 consecutive patients admitted to Assaf Harofeh Medical Center during 2009, and scheduled to undergo coronary catheterization was undertaken. Blood was collected for parathyroid hormone, 25(OH)D and high sensitivity C reactive protein (hsCRP). 25(OH)D deficiency was defined as <20 ng/ml. Patients were divided into two groups: patients with normal or non-significant coronary artery disease and patients with a significant coronary artery disease as found during cardiac catheterization. Logistic regression model was used to compare pathological coronary catheterization findings, including 25(OH)D levels dichotomized to low (serum 25(OH)D levels<20 ng/ml) vs. high (serum 25(OH)D levels ≥ 20 ng/ml) and other confounders. RESULTS: Patients with pathological coronary catheterization had 25(OH)D deficiency (75% vs 55.1%, p=0.036). Pathological coronary catheterization was more prevalent among patients with 25(OH)D deficiency (Odds ratio (OR) 2.44, 95% confidence interval (CI) 1.05-5.68, p=0.038). This difference was more pronounced after controlling for sex, age, BMI, ethnicity and present smoking (OR 2.92, 95% CI 1.01-8.46, p=0.016). CONCLUSIONS: 25(OH)D deficiency is significantly associated with pathological cardiac catheterization findings. This association is strengthened further by controlling for other cardiovascular disease risk factors.

A highly unusual right atrial mass presented in two women.

Intravenous leiomyomatosis is a rare, benign neoplasm of the uterine, affecting adult women. We report two cases in whom intravenous leiomyomatosis extended through the inferior vena cava into the right heart chambers and the pulmonary artery. Both patients underwent staged operation with excision of the cardiac and primary tumour. The differential diagnosis of a right atrial mass in middle-aged women should include intravenous leiomyomatosis.

Tezosentan (an intravenous endothelin receptor A/B antagonist) reduces peripheral resistance and increases cardiac power therefore preventing a steep decrease in blood pressure in patients with congestive heart failure.

OBJECTIVE: This study investigated the effect of tezosentan (an intravenous endothelin-1 receptor antagonist) on vascular resistance and cardiac function and determined the dose response in patients with stable congestive heart failure (CHF) due to left ventricular systolic dysfunction. METHODS: In a double-blind fashion, tezosentan or placebo were administered in ascending doses (5, 20, 50, 100 mg h(-1)) to 38 CHF (NYHA class III) patients with ejection fraction or=15 mmHg. Systemic vascular resistance index (SVRi) was estimated as mean arterial blood pressure [(MAP-right atrial pressure)/cardiac index (CI)]. Cardiac function was assessed as cardiac power index (Cpi), calculated as pressure x flow (MAP x CI), where MAP represents pressure and CI represents cardiovascular flow. RESULTS AND DISCUSSION: Compared to the placebo, tezosentan induced a dose-dependent decrease in SVRi (-32%), an increase in Cpi (+20%) and a small decrease in MAP (-9%). By contrast, patients treated with nitrate vasodilators or nesiritide (a natriuretic peptide) showed a decrease in SVRi not accompanied by a significant increase in Cpi leading to a steep decrease in MAP. CONCLUSIONS: The use of Cpi in the assessment of the hemodynamic effects of tezosentan, provides a useful alternative characterization of the complex influences of vasodilators on cardiac function in patients with CHF.

Pulmonary edema: new insight on pathogenesis and treatment.

Pulmonary edema is one of the most serious and life-threatening situations in emergency medicine. Lately it has become apparent that in most cases pulmonary edema is not caused by fluid accumulation but rather fluid redistribution that is directed into the lungs because of heart failure. Based on a series of recently published studies, we propose that often the pathogenesis of pulmonary edema is related to a combination of marked increase in systemic vascular resistance superimposed on insufficient systolic and diastolic myocardial functional reserve. This resistance results in increased left ventricular diastolic pressure causing increased pulmonary venous pressure, which yields a fluid shift from the intravascular compartment into the pulmonary interstitium and alveoli, inducing the syndrome of pulmonary edema. Therefore, the emphasis in treating pulmonary edema has shifted from diuretics (ie, furosemide) to vasodilators (ie, high-dose nitrates) combined with noninvasive positive airway pressure ventilation and rarely inotropes. New classes of drugs that are currently being investigated for treating decompensated heart failure such as natriuretic peptides, calcium promoters, and endothelin antagonist are also being assessed for treating pulmonary edema. This review will explore this new hypothesis put forward to explain the pathogenesis of pulmonary edema and the evolving management strategies.

Stents in total occlusion for restenosis prevention. The multicentre randomized STOP study. The Israeli Working Group for Interventional Cardiology.

AIMS: This multicentre randomized study set out to evaluate whether coronary stenting improves the results of successful balloon angioplasty for chronic total occlusion. Balloon angioplasty for chronic total occlusion has a high restenosis rate. Several reports have suggested that coronary stenting may decrease the likelihood of restenosis and reocclusion. METHODS AND RESULTS: Patients with total coronary artery occlusions who had an optimal PTCA result were randomized either to no further treatment or additional stent implantation. The AVE microstent was used and all patients were scheduled for a 1-, 3-, and 6-month clinical follow-up. Repeat coronary angiography to assess the rate and pattern of restenosis was performed at 6 months or earlier if clinically indicated. Ninety-six patients were enrolled in this study. The mean age was 59. 3+/-10.3 years and 15 were females. Forty-eight patients were randomized to the stent arm, receiving 52 stents (lengths 18-39 mm). Stent implantation was successful in all and there were no major procedure-related complications. Sixty-nine patients (72%) were restudied after 6 months. The binary restenosis rates (50%), in the PTCA arm were 70.9% with a minimal lumen diameter of 1.01+/-0.79 mm compared to 42.1% in the stent arm with a minimal lumen diameter of 1.63+/-1.02 mm (P=0.034). Reocclusion occurred in 7.9% in the stent group compared to 16.1% in the PTCA group. Restenosis in the PTCA group was focal in 88% of patients and occurred at the point of total obstruction (within 5 mm), compared to diffuse instent restenosis, which occurred in 54% of the patients in the stent group. CONCLUSION: Coronary stenting can significantly decrease the rate of restenosis and reocclusion of total occlusions. As restenosis in the stent group was more diffuse, care should be taken to implant short stents at the site of occlusion.

High-dose intravenous isosorbide-dinitrate is safer and better than Bi-PAP ventilation combined with conventional treatment for severe pulmonary edema.

OBJECTIVE: To determine the feasibility, safety and efficacy of bilevel positive airway ventilation (BiPAP) in the treatment of severe pulmonary edema compared to high dose nitrate therapy. BACKGROUND: Although noninvasive ventilation is increasingly used in the treatment of pulmonary edema, its efficacy has not been compared prospectively with newer treatment modalities. METHODS: We enrolled 40 consecutive patients with severe pulmonary edema (oxygen saturation <90% on room air prior to treatment). All patients received oxygen at a rate of 10 liter/min, intravenous (IV) furosemide 80 mg and IV morphine 3 mg. Thereafter patients were randomly allocated to receive 1) repeated boluses of IV isosorbide-dinitrate (ISDN) 4 mg every 4 min (n = 20), and 2) BiPAP ventilation and standard dose nitrate therapy (n = 20). Treatment was administered until oxygen saturation increased above 96% or systolic blood pressure decreased to below 110 mm Hg or by more than 30%. Patients whose conditions deteriorated despite therapy were intubated and mechanically ventilated. All treatment was delivered by mobile intensive care units prior to hospital arrival. RESULTS: Patients treated by BiPAP had significantly more adverse events. Two BiPAP treated patients died versus zero in the high dose ISDN group. Sixteen BiPAP treated patients (80%) required intubation and mechanical ventilation compared to four (20%) in the high dose ISDN group (p = 0.0004). Myocardial infarction (MI) occurred in 11 (55%) and 2 (10%) patients, respectively (p = 0.006). The combined primary end point (death, mechanical ventilation or MI) was observed in 17 (85%) versus 5 (25%) patients, respectively (p = 0.0003). After 1 h of treatment, oxygen saturation increased to 96 +/- 4% in the high dose ISDN group as compared to 89 +/- 7% in the BiPAP group (p = 0.017). Due to the significant deterioration observed in patients enrolled in the BiPAP arm, the study was prematurely terminated by the safety committee. CONCLUSIONS: High dose ISDN is safer and better than BiPAP ventilation combined with conventional therapy in patients with severe pulmonary edema.

Minimal heparinization in coronary angioplasty--how much heparin is really warranted?

The purpose of the study was to assess the results of percutaneous transluminal coronary angioplasty (PTCA), performed with a single intravenous bolus of 2,500 U of heparin, in a nonemergency PTCA cohort. Three hundred of 341 consecutive patients (87.9%) undergoing PTCA were prospectively enrolled in the study. They received heparin, 2,500-U intravenous bolus, before PTCA, with intention of no additional heparin administration. Patient and lesion characteristics as well as PTCA results were evaluated independently by 2 physicians. Patients were followed up by structured telephone questionnaires at 1 and 6 months after PTCA. Mean activated clotting time obtained 5 minutes after heparin administration was 185+/-19 seconds (range 157 to 238). There were 3 (1%) in-hospital major adverse cardiovascular events: 2 deaths (0.66%), 1 (0.33%) Q-wave myocardial infarction. Emergency coronary surgery and stroke were not reported. Six patients (2%) experienced abrupt coronary occlusion within 14 days after PTCA, warranting repeat target vessel revascularization. Angiographic and clinical success were achieved in 96% and 93.3%, respectively. No bleeding or vascular complications were recorded. Six-month follow-up (184 patients) revealed 3 cardiac deaths (1 arrhythmic, 2 after cardiac surgery), 1 Q-wave myocardial infarction, and 9.7% repeat target vessel revascularization. This study suggests that very low doses of heparin and reduced activated clotting time target values are safe in non-emergency PTCA, and can reduce bleeding complications, hospital stay, and costs. Larger, randomized, double-blind heparin dose optimization studies need to confirm this notion.

A right atrial mass in the presence of a permanent pacemaker electrode in a patient with polycythemia vera.

A case of a huge right atrial mass that developed 2 years after a permanent pacemaker implantation is described. The patient had a history of polycythemia vera, which is known to present a high tendency towards the development of thrombosis. In light of this fact, we suggest that in similar cases a full echocardiography follow-up should be performed, and long-term anticoagulant therapy should be considered in selected cases.

Early thrombolytic therapy does not enhance the recovery of the right ventricle in patients with acute inferior myocardial infarction and predominant right ventricular involvement.

In this study we report the effects of early thrombolytic therapy on the recovery of the right ventricle after an acute myocardial infarction. Sixty-five patients presenting with their first inferior myocardial infarction and predominant right ventricular involvement were consecutively treated as follows: group A (20 patients) conservatively (without thrombolytic therapy), group B (19 patients) with streptokinase and group C (26 patients) with recombinant tissue type plasminogen activator. Coronary angiography was performed within 72 h after admission in 52 patients (10 of group A, 18 of group B and in 24 patients of group C) followed by transluminal coronary angioplasty in 26. All groups had similar characteristics except for a higher mean age in group A. Within 3 months, a remarkable improvement in right ventricular function and a major increase in ejection fraction was observed for all three patient groups. Improvement of right ventricular function was more prominent in patients with residual flow through the infarct-related artery. The beneficial course was comparable in all the groups, unaffected by the type of medical treatment applied, or by the performance of coronary angioplasty. No further significant change occurred beyond this period. Thus, early thrombolytic therapy does not augment the generally favorable course of recovery of the right ventricle from acute infarction.