Hemodynamics of Stent Implantation Procedures in Coronary Bifurcations: An <Emphasis Type="Italic">In Vitro</Emphasis> Study

Stent implantation in coronary bifurcations presents unique challenges and currently there is no universally accepted stent deployment approach. Despite clinical and computational studies, the effect of each stent implantation method on the coronary artery hemodynamics is not well understood. In this study the hemodynamics of stented coronary bifurcations under pulsatile flow conditions were investigated experimentally. Three implantation methods, provisional side branch (PSB), culotte (CUL), and crush (CRU), were investigated using time-resolved particle image velocimetry to measure the velocity fields. Subsequently, hemodynamic parameters including wall shear stress, oscillatory shear index (OSI), and relative residence time (RRT) were calculated. The pressure field through the vessel was non-invasively quantified and pressure wave speeds were computed. The effects of each stented case were evaluated and compared against an un-stented case. CRU provided the lowest compliance mismatch, but demonstrated detrimental stent interactions. PSB, the clinically preferred method, and CUL maintained many normal flow conditions. However, PSB provided about a 300% increase in both OSI and RRT. CUL yielded a 10 and 85% increase in OSI and RRT, respectively. The results of this study support the concept that different bifurcation stenting techniques result in hemodynamic environments that deviate from that of un-stented bifurcations, to varying degrees.     

An integrated assessment of family history on the risk of developing acute coronary syndromes (CARDIO2000 study)

OBJECTIVE: In this work we assessed a risk score for developing a first event of acute coronary syndrome (ACS) based on the family history of the cardiovascular risk factors. METHODS AND RESULTS: The studied population consisted of 848 randomly selected middle-aged patients with first event of ACS and 1078 sex-age-region matched controls admitted to the same hospitals for minor operations and without any clinical suspicion of cardiovascular disease in their life. A Family History Score (FHS) was developed based on the presence of coronary heart disease, hypertension, hypercholesterolaemia and diabetes mellitus, among first-degree relatives of the participants after adjusting for the family size. The evaluation of FHS was based on conditional logistic regression analysis, after controlling for demographic variables as well as for the mutual confounding effects of other risk factors. Family history of CHD, hypercholesterolaemia and diabetes was highly associated with the development of the disease. The introduced FHS was also highly associated with the development of ACS among participants who had no family history of CHD (odds ratio = 10.9, p < 0.001), whereas it was not associated with the development of the disease among participants who had a family history of CHD (odds ratio = 1.41, p = 0.543). CONCLUSIONS: The suggested FHS could be a useful tool in the primary prevention of ACS, as well as in detecting and understanding associations between genetic vulnerability and cardiovascular risk factors.     

Plasma level changes of fibrinopeptide a after uncomplicated coronary angioplasty

Fibrinopeptide A (FPA) is a small polypeptide cleaved from fibrinogen by thrombin, has a short half-life, and is considered a sensitive biochemical marker of thrombin activity, fibrin generation, and ongoing thrombosis. Increased plasma levels of FPA have been reported in various procoagulable and thrombotic medical and cardiovascular disorders, including acute myocardial infarction, unstable angina, and sudden cardiac death. However, activation of thrombosis by the arterial injury incurred during coronary angioplasty has not been systematically examined with use of plasma FPA measurements. To detect and monitor activation of thrombosis by coronary angioplasty, plasma levels of FPA were obtained by venipuncture and measured by radioimmunoassay before, immediately after, 24 to 48 h later, and 1 and 3 months after uncomplicated coronary angioplasty. From December 1990 through June 1991, FPA was measured in 30 patients (28 men and 2 women, aged 54 ± 9 years) with coronary artery disease who were undergoing coronary angioplasty. The mean left ventricular ejection fraction was 55 ± 7%. The dilated vessel was the left anterior descending coronary artery in 20 patients (together with a second vessel in 2), the right coronary artery in 9, and the left circumflex in 1. The procedure was successful and free of major complications in all patients. Before angioplasty the FPA levels averaged 6.50 ± 1.18 ng/ml. Shortly after angioplasty they rose to 20.20 ± 7.91 ng/ml (p = 0.08) despite intravenous heparin. At 24 to 48 h and after heparin had been discontinued for at least 4 h, the mean FPA levels were significantly higher (32.33 ± 10.86 ng/ml) compared with baseline values (p = 0.025 ). At 1 month after the procedure, the FPA levels measured in 22 patients were lower but still elevated (20.25 ± 9.29 ng/ml), albeit nonsignificantly, compared with baseline values, and at 3 months they had fallen to baseline values (4.84 ± 2.20 ng/ml, n = 11). No patient developed restenosis during the study period of 1 to 3 months, during which all patients were receiving aspirin. We conclude that, as reflected by increased FPA levels, angioplasty, most likely due to arterial injury incurred, activates thrombin and generates ongoing coronary thrombosis, which is not suppressed by heparin or aspirin and appears to extend at least through the first month after the procedure.     

Isolated native tricuspid valve Candida endocarditis in a non-drug-addicted patient: case report and review of the literature

A case is reported of isolated native tricuspid calve Candida parapsilosis endocarditis (INTVCE) in a male patient with no history of drug abuse or heart disease. The patient had received hyperalimentation and antibiotics for four months via a central venous catheter after abdominal surgery. He underwent successful treatment with tricuspid valve debridement, liposomal amphotericin (AmBisome) and fluconazole, and remained without relapse during an eight-year follow up. A literature review of 12 similar cases (including the present patient) without history of drug abuse or heart disease, dating from 1970, is included.     

Clinical features of hypertrophic cardiomyopathy caused by an Arg278Cys missense mutation in the cardiac troponin T gene

To further examine the genetic and clinical features of hypertrophic cardiomyopathy caused by mutations in the cardiac troponin T (cTnT) gene, we screened 143 probands from our hypertrophic cardiomyopathy population for mutations in this gene. We report that the Arg278Cys missense mutation in the cTnT gene had a different clinical presentation in 2 different families and was associated with a clinical profile that deviates from what is currently expected for cTnT gene mutations.     

Association between passive cigarette smoking and the risk of developing acute coronary syndromes: the CARDIO2000 study

Although the effect of smoking on human health has been established as a major risk factor, the effect of passive smoking is controversial. The purpose of this study was to investigate the association between passive smoking and the risk of acute coronary syndromes (ACS) among nonsmokers. Eight hundred and forty-eight patients with the first event of ACS and 1078 cardiovascular disease-free matched controls completed a detailed questionnaire regarding their exposure to environmental smoke. Two hundred and ninety-seven (35%) of the patients and 259 (24%) of the controls were defined as nonsmokers and passive smokers, respectively. After controlling for several potential confounders, the results showed that nonsmokers exposed to cigarette smoke increased the risk of ACS by 51% (odds ratio = 1.51, 95% confidence interval 1.21–2.99) compared with nonsmokers not exposed to smoke. It was estimated that 34 coronary events per 134 subjects would occur as a result of passive smoking during their lifetime. Consequently, this study supports the hypothesis that passive smoking increases the risk of developing acute coronary syndromes. Given the high prevalence of cigarette smoking in many developing societies, the public health consequences of passive smoking with regard to coronary heart disease may be important. Received: November 19, 2001 / Accepted: January 25, 2002     

Hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption

Acid-base disturbances, such as metabolic or respiratory alkalosis, are relatively common in critically ill patients. We examined the effects of alkalosis (hypocapnic or metabolic alkalosis) on alveolar fluid reabsorption in the isolated and continuously perfused rat lung model. We found that alveolar fluid reabsorption after 1 hour was impaired by low levels of CO2 partial pressure (PCO2; 10 and 20 mm Hg) independent of pH levels (7.7 or 7.4). In addition, PCO2 higher than 30 mm Hg or metabolic alkalosis did not have an effect on this process. The hypocapnia-mediated decrease of alveolar fluid reabsorption was associated with decreased Na,K-ATPase activity and protein abundance at the basolateral membranes of distal airspaces. The effect of low PCO2 on alveolar fluid reabsorption was reversible because clearance normalized after correcting the PCO2 back to normal levels. These data suggest that hypocapnic but not metabolic alkalosis impairs alveolar fluid reabsorption. Conceivably, correction of hypocapnic alkalosis in critically ill patients may contribute to the normalization of lung ability to clear edema.     

Vulnerable plaque: the challenge to identify and treat it

In order to understand, treat, and prevent acute coronary syndromes we need to improve our ability to identify the rupture-prone, vulnerable atherosclerotic coronary plaque. The diagnostic modalities that are currently available to clinical practice have not fulfilled this expectation, and newer diagnostic techniques based on the recently identified features of the vulnerable plaque are quite promising. Coronary angiography, intravascular ultrasound, and angioscopy have been used in the clinical arena of interventional cardiology with several limitations regarding the identification of the vulnerable plaque. Thermography, optical coherence tomography, elastography, Raman spectroscopy, and infrared spectroscopy are used in clinical trials and the results are encouraging. Ultrafast computed tomography and magnetic resonance imaging have the advantage of being noninvasive. With our progress in the identification of the rupture-prone vulnerable coronary plaque, we will be able to identify patients that are at high risk and will benefit from a more aggressive therapeutic approach.