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Manolis Vavuranakis

Publications and source records attributed to Manolis Vavuranakis.

At least 19 recordsLinked to original sources
PubMed2006

Spontaneous coronary dissection as a cause of acute coronary syndrome: evidence for non-inflammatory underlying mechanisms.

Myocardial infarction in patients without atherosclerotic coronary artery disease is a rare syndrome. Several pathophysiologic mechanisms have been proposed, such as spontaneous coronary dissection, intramural hematoma, coronary vasospasm and thrombosis. Diagnosis can be confirmed by coronary angiography and intravascular ultrasound, while the presence of an inflammatory process within the coronary artery wall can be detected from local heat production by intracoronary thermography. We present two women with acute coronary syndrome, due to a limited spontaneous coronary dissection and an intramural hematoma detected by coronary angiography and intravascular ultrasound.

Acute Disease↗
PubMed2006

Alterations of pressure waveforms along the coronary arteries and the effect of microcirculatory vasodilation.

OBJECTIVES: We sought to investigate the differences of pressure waveforms at a distal point of an epicardial coronary artery comparatively to the ostium and to assess the effect of microcirculatory vasodilation on them. BACKGROUND: Pressure waveforms in the systematic circulation and their alterations along the aorta due to wave reflections from the periphery have been extensively studied. However, similar data regarding intracoronary pressure waveforms and the effects of coronary microcirculation on them are limited. METHODS: In 18 patients who underwent diagnostic coronary angiogram or percutaneous coronary intervention in the left circumflex or the right coronary artery, we studied pressure waveforms recorded by a high-fidelity pressure wire, which was advanced to the ostium and to a distal site of the free of significant lesions left anterior descending coronary artery. Pressure recording was performed both at rest and at hyperemia induced by intravenous infusion of adenosine. Analysis of pressure waveforms at the frequency domain was performed with Fast Fourier Transform. RESULTS: At baseline conditions, distal pressure waveforms were characterized by higher pulsatility, higher presystolic wave and higher amplitude of the 11th to the 15th harmonics. Hyperemia increased the pulsatility, compressed the notch and decreased the amplitude of higher than the 10th harmonics of distal waveforms. CONCLUSIONS: This study identifies differences of pressure waveforms between proximal and distal sites of free of significant lesions coronary arteries, which are affected by the status of coronary microcirculation and may therefore facilitate assessment of microvascular disease.

Adenosine↗
PubMed2006

Assessment of vascular wall shear stress and implications for atherosclerotic disease.

Mechanical characteristics of circulation and vasculature, such as blood flow in combination with geometrical features, participate in the generation of several pathophysiological processes, such as development of blood vessel structure, chronic vessel tone regulation, atherosclerosis and others. We aim to briefly describe the basic mechanical and haemodynamic phenomena related to the forces applied to arterial walls, especially shear stresses and the shear-induced physiologic and pathophysiologic processes focusing on those related to atherosclerotic disease.

Atherosclerosis↗
PubMed2006

Relation between local temperature and C-reactive protein levels in patients with coronary artery disease: effects of atorvastatin treatment.

Although previous studies have shown systemic inflammatory activation the relation with the local plaque inflammatory activation has not been extensively studied. The present study investigated the relation between local and systemic inflammatory activation in patients with coronary artery disease and the impact of atorvastatin treatment. We included 215 patients undergoing percutaneous coronary intervention; of them 140 were treated with atorvastatin. Patients with stable angina (SA) and acute coronary syndromes (ACS) were included. Systemic inflammation was assessed by serum C-reactive protein (CRP), soluble adhesion molecules levels and local plaque inflammatory activation by coronary thermography. Temperature difference (DeltaT) was assigned as the difference between the proximal vessel wall temperature from the maximal temperature at the culprit plaque. Patients with ACS (n=78) had increased DeltaT compared to patients with SA (n=137) (0.16+/-0.10 degrees C versus 0.08+/-0.07 degrees C, P<0.001). Patients treated with atorvastatin had lower DeltaT compared to untreated patients (0.10+/-0.07 degrees C versus 0.15+/-0.10 degrees C, P<0.01). DeltaT was less in the treated group compared to the untreated group in patients with SA and ACS (ACS: 0.13+/-0.08 degrees C versus 0.20+/-0.11 degrees C, P<0.01, SA: 0.08+/-0.06 degrees C versus 0.13+/-0.08 degrees C, P=0.03). Although a correlation was found between CRP levels and DeltaT (R=0.29, P<0.01), in certain groups a discrepancy between CRP levels and DeltaT was observed. In 25% of patients with low DeltaT CRP levels were >1mg/dl and in 35.5% of patients with high DeltaT CRP was <2mg/dl. The correlation between soluble adhesion molecules and DeltaT did not reach statistical significance. Although there is a correlation between widespread and local inflammatory activation in patients with coronary artery disease, a discrepancy between culprit plaque and systemic inflammatory activation is observed. Atorvastatin has a parallel effect on systemic and local inflammatory process in patients with coronary artery disease.

Aged↗
PubMed2006

Differences in inflammatory and thrombotic markers between unstable angina and acute myocardial infarction.

BACKGROUND: Unstable coronary syndromes are characterised by increased inflammatory process and endothelial activation. However, the underlying mechanisms of the acute coronary syndromes are still obscure. We evaluated the differences of inflammatory and thrombotic markers, at the acute phase of unstable angina (UA) and acute myocardial infarction (AMI). METHODS: The population of the study consisted of 216 subjects: 136 patients with UA, 57 patients with AMI and 23 healthy controls. Blood samples were taken by their admission to the hospital. Inflammatory and thrombotic markers were measured by ELISA. RESULTS: Patients with UA had significantly higher levels of interleukin-6 (IL-6), soluble vascular cells adhesion molecule (sVCAM-1) and von Willebrand factor (vWF) (p<0.05 vs controls), and lower levels of antithrombin III (ATIII) (p<0.01 vs controls) and protein C (PrtC) (p<0.05 vs controls). Similarly, patients with AMI had higher levels of IL-6, sVCAM-1, vWF and tissue plasminogen activator (tPA) (p<0.01 vs controls) and lower levels of ATIII (p<0.01 vs controls) and prtC (p<005 vs controls). Patients with AMI had significantly higher levels of vWF, tPA and sVCAM-1 compared to UA patients (p<0.05). CONCLUSIONS: Patients with unstable coronary syndromes had increased levels of IL-6, sVCAM-1 and vWF as well as decreased levels of ATIII and PrtC by their admission. However, patients with AMI had higher levels of all the endothelium-derived inflammatory (e.g. sVCAM-1) of thrombotic/fibrinolytic (e.g. tPA and vWF) markers, compared to those with UA. These findings imply that patients with myocardial infarction show further increase of endothelium-derived inflammatory and thrombotic markers compared to patients with unstable angina, in response to a similar proinflammatory stimuli.

Angina, Unstable↗
PubMed2006

Elevated plaque temperature in non-culprit de novo atheromatous lesions of patients with acute coronary syndromes.

OBJECTIVES: We investigated whether there is increased temperature in non-culprit lesions, and the correlation of clinical syndrome with heat production of non-culprit lesions. BACKGROUND: There is a controversy regarding whether there is widespread inflammation involving non-culprit lesions, or whether inflammatory involvement is limited to the culprit lesion. Coronary thermography assesses the local inflammatory involvement in atherosclerotic lesions. METHODS: We included patients suffering from stable angina (SA) or acute coronary syndrome (ACS). All patients had two or more angiographically detectable lesions at different arteries. Culprit lesions should be identified in all patients. Patients with chronic total occlusions and multiple significant lesions at the culprit vessel were excluded. We measured at each non-culprit lesion the temperature difference (DeltaT) between the atherosclerotic plaque and the proximal vessel wall temperature. RESULTS: The study population included 42 patients: 23 with SA, 19 with ACS. The DeltaT in non-culprit lesions was 0.08 +/- 0.07 degrees C. Patients with ACS had a higher temperature difference in non-culprit lesions compared with patients with SA (ACS 0.11 +/- 0.08 degrees C vs. SA 0.05 +/- 0.06 degrees C; p < 0.01). The mean value of DeltaT in non-culprit lesions was higher in the untreated group compared with the treated group with statins (0.11 +/- 0.10 degrees C vs. 0.06 +/- 0.05 degrees C; p = 0.05). CONCLUSIONS: The results of this study show that heat is generated in non-culprit lesions. Moreover, in patients with ACS, temperature difference is increased compared with patients with stable angina.

Aged↗
PubMed2006

Randomized comparison of the effects of ASA plus clopidogrel versus ASA alone on early platelet activation in acute coronary syndromes with elevated high-sensitivity C-reactive protein and soluble CD40 ligand levels.

BACKGROUND: High-sensitivity C-reactive protein (hsCRP) and soluble cluster of differentiation 40 ligand (sCD40L) have been established as effective markers of inflammation in predicting the risk for adverse outcomes in patients with acute coronary syndromes (ACSs). Activated platelets secrete certain inflammatory mediators such as P-selectin and sCD40L, which play a role in the pathogenesis of ACSs. Although acetylsalicylic acid (ASA) has been found to be an effective treatment of ACSs, the addition of clopidogrel bisulfate has been found tofurther improve clinical outcomes as a result of additional antiplatelet and anti-inflammatory action. Few data exist concerning the effects of dual antiplatelet therapy on these markers in patients with ACSs. OBJECTIVE: The aim of this study was to assess the effectiveness and clinical significance of clopidogrel administration in patients with ACSs without ST segment elevation treated with ASA. METHODS: This randomized, single-blind, controlled trial was conducted at the First Department of Cardiology, Hippokration Hospital, Athens, Greece. Inpatients aged>or=21 years with ACSs without ST segment elevation were randomly assigned to 1 of 2 groups: ASA 325 mg/d for 1 week, followed by ASA (100 mg/d) plus clopidogrel (300-mg loading dose followed by 100 mg/d) for 36 weeks (ASA+Clop group) or ASA alone (325 mg/d for 1 week, followed by 75 mg/d for 36 weeks) (ASA group). Levels of serum sCD40L, hsCRP, and P-selectin were determined on admission and at 8 hours, 48 hours, and 6 days of treatment. By means of clinical follow-up, Kaplan-Meier free-of-major adverse cardiovascular events (MACES) plots were used to assess the prevalence of MACES, including cardiovascular-related death, in patients with and without high levels of hsCRP (>or=3 mg/L) and sCD40L (>or=5 microg/L) for 52 weeks. RESULTS: A total of 86 patients were enrolled (71 men, 15 women; mean [SD] age, 68 [3] years; mean [SD] weight, 86 [18] kg; white race, 86 [100%]; 43 patients per group). Both groups had similar initial clinical characteristics and P-selectin levels. Baseline hsCRP and sCD40L levels were correlated with baseline P-selectin levels (hsCRP, r2=0.099 CONCLUSIONS: The results of this small study suggest that early activation of platelets, as measured using P-selectin levels, was effectively inhibited by the addition of clopidogrel to a regimen of ASA in the subgroup of patients with ACSs and intense activation of platelets (defined as high hsCRP and sCD40L levels). In patients without high hsCRP and sCD40L levels, the addition of clopidogrel did not have a significant effect on P-selectin levels.

Acute Disease↗
PubMed2006

Right ventricular infarction mimicking anterior infarction.

It is rare to observe ST elevation in anterior derivations caused by right ventricular branch occlusion. We described the case of a patient with unstable angina who developed acute right ventricular myocardial infarction with ST-segment elevation in anterior precordial leads (V(1)-V(4)) shortly after coronary angiography. Coronary angiogram revealed total occlusion of the right coronary artery (RCA) proximally to the right ventricular branch. This reminds us that the presence of diffuse ST-segment elevation in the precordial leads could be due to acute RCA occlusion. The differentiation of these two entities is important, as their therapies are quite different.

Angina, Unstable↗
PubMed2006

Torsades de pointes as a cause of sudden death in a patient with aortic stenosis and atrial fibrillation.

The occurrence of sudden cardiac death during Holter monitoring in patients with aortic stenosis has been reported previously. In the majority of the reported cases, the cause of death was a malignant ventricular tachyarrhythmia. The presence of a strong association between frequency and complexity of ventricular arrhythmias and sudden death in patients with aortic stenosis has been proposed. We report the case of a 77-year-old woman with aortic stenosis and atrial fibrillation who had an episode of torsades de pointes that degenerated into ventricular fibrillation during Holter monitoring. A short-long-short sequence, but not increased ventricular ectopics, precipitated torsades de pointes and sudden death in this case which is strongly indicative of triggered activity as the underlying mechanism of the lethal arrhythmia.

Aged↗
PubMed2005

Intravascular ultrasound-based imaging of vasa vasorum for the detection of vulnerable atherosclerotic plaque.

Vulnerable plaques are dangerous atherosclerotic lesions that bear a high risk of complications that can lead to heart attacks and strokes. These plaques are known to be chronically inflamed. The vasa vasorum (VV) are microvessels that nourish vessel walls. Proliferation of VV is part of the "response to injury" phenomenon in the process of plaque formation. Recent evidence has shown strong correlations between neovessel formation and macrophage infiltration in atherosclerotic plaque, suggesting VV density as a surrogate marker of plaque inflammation and vulnerability. We have developed a novel method for imaging and analyzing the density and perfusion of VV in human coronary atherosclerotic plaques using intravascular ultrasound (IVUS). Images are taken during the injection of a microbubble contrast agent and the spatiotemporal changes of the IVUS signal are monitored using enhancement-detection techniques. We present analyses of in vivo human coronary cases that, for the first time, demonstrate the feasibility of IVUS imaging of VV.

Coronary Artery Disease↗
PubMed2005

Vasa vasorum imaging: a new window to the clinical detection of vulnerable atherosclerotic plaques.

Complications of vulnerable atherosclerotic plaques (rupture, luminal and mural thrombosis, intraplaque hemorrhage, rapid progression to stenosis, spasm, and so forth) lead to heart attacks and strokes. It remains difficult to identify what plaques are vulnerable to these complications. Despite recent developments such as thermography, spectroscopy, and magnetic resonance imaging, none of them is approved for clinical use. Intravascular ultrasound (IVUS), a relatively old yet widely available clinical tool for guiding intracoronary procedures, is increasingly used for characterization of atherosclerotic plaques. However, inability of IVUS in measuring plaque activity limits its value in detection of vulnerable plaques. In this review, we present new information suggesting that microbubble contrast-enhanced IVUS can measure activity and inflammation within atherosclerotic plaques by imaging vasa vasorum density. An increasing body of evidence indicates that vasa vasorum density may be a strong marker for plaque vulnerability. We suggest that a combination of structural assessment (cap thickness, lipid core, calcification, etc) and vasa vasorum density imaging by IVUS can serve as the most powerful clinically available tool for characterization of vulnerable plaques. Due to space limitations, all IVUS images and movies are posted on the website of the Ultimate IVUS Collaborative Project: http://www.ultimateivus.com.

Albumins↗
PubMed2005

Increased heat generation from atherosclerotic plaques in patients with type 2 diabetes: an increased local inflammatory activation.

OBJECTIVE: Patients with coronary artery disease (CAD) and diabetes show increased inflammatory activation. Thermography detects local inflammatory involvement as heat generation. The aim of this study was to investigate whether patients with CAD and diabetes have increased local heat generation compared with nondiabetic patients. RESEARCH DESIGN AND METHODS: We enrolled patients undergoing percutaneous coronary interventions: 45 diabetic patients and 63 nondiabetic patients, serving as the control group, matched for age, type of clinical syndrome, statin and aspirin intake, and angiographic stenosis (%). Coronary thermography was performed, and temperature difference (DeltaT) between the atherosclerotic plaque and the proximal vessel wall was measured. RESULTS: Patients with diabetes had increased temperature difference compared with nondiabetic patients (DeltaT: 0.17 +/- 0.18 degrees C vs. 0.09 +/- 0.02 degrees C, P = 0.01). Twenty-one diabetic and 22 nondiabetic patients suffered from acute coronary syndromes (ACSs) (P = 0.22). Patients with diabetes and ACSs had increased temperature difference compared with nondiabetic patients with ACSs (DeltaT: 0.29 +/- 0.31 degrees C vs. 0.15 +/- 0.21 degrees C, P = 0.02), which is the same as patients with diabetes and chronic stable angina (DeltaT: 0.09 +/- 0.08 degrees C vs. 0.05 +/- 0.04 degrees C, P = 0.006). Twenty-three diabetic and 30 nondiabetic patients were under therapy with statins (P = 0.72). Patients with diabetes under statins had lower temperature difference compared with untreated patients (DeltaT: 0.11 +/- 0.12 degrees C vs. 0.22 +/- 0.21 degrees C, P = 0.02), which is the same as nondiabetic patients under statins (DeltaT: 0.05 +/- 0.04 degrees C vs. 0.13 +/- 0.18 degrees C, P = 0.01). CONCLUSIONS: Patients with diabetes have increased temperature difference compared with nondiabetic patients. Patients with diabetes under statins showed decreased temperature difference compared with untreated patients, suggesting that statins have a favorable effect in patients with diabetes and CAD.

Angioplasty, Balloon, Coronary↗
PubMed2004

Detection of increased temperature of the culprit lesion after recent myocardial infarction: the favorable effect of statins.

BACKGROUND: Increased thermal heterogeneity has been demonstrated in atherosclerotic plaques, with the higher temperature recorded in acute myocardial infarction (MI). Dietary or treatment interventions reduce heat production. The purpose of the present study was to investigate whether increased plaque temperature is maintained for a prolonged period after MI and the role of statin administration. METHODS: We enrolled 55 patients, 29 with recent MI and 26 with chronic stable angina (CSA). Total cholesterol, C-reactive protein (CRP), interleukin-6 (IL-6) and soluble adhesion molecules were measured in the study population. All patients underwent coronary plaque temperature measurements. Temperature difference (DeltaT) was designated as the temperature of the culprit atherosclerotic plaque minus the temperature of the proximal healthy vessel wall. RESULTS: Under treatment with statins were 19 patients with recent MI and 14 with CSA. In patients with recent MI DeltaT was 0.19 +/- 0.18 degrees C, while in patients with CSA was 0.10 +/- 0.08 degrees C (P = .03). Patients treated with statins had lower DeltaT compared to untreated patients (0.10 +/- 0.11 versus 0.20 +/- 0.18 degrees C, P = .01). Treated patients with recent MI had similar DeltaT compared to CSA patients treated with statins (0.13 +/- 0.13 versus 0.07 +/- .06 degrees C, P = .14), while untreated patients with recent MI had substantially increased DeltaT compared to untreated patients with CSA (0.28 +/- 0.22 versus 0.14 +/- 0.10 degrees C, P = .04). DeltaT was positively correlated with CRP (R = 0.50, P < .01), IL-6 (R = 0.58, P < .01), and intercellular adhesion molecule-1 (R = 0.40, P = .03) levels. CONCLUSION: Increased plaque temperature is observed for an extended period after myocardial infarction, indicating that the inflammatory process is sustained after plaque rupture. Statins have a beneficial effect after MI on plaque temperature.

Aged↗
PubMed2004

Lack of increased left main coronary artery dimensions in hypertensive patients with left ventricular hypertrophy and coronary artery disease. An intracoronary ultrasound study.

OBJECTIVES: Left main coronary artery dimensions were evaluated in patients with and without arterial hypertension, in the presence of coronary artery disease, and correlated to left ventricular mass. METHODS AND RESULTS: Intracoronary ultrasound was performed in 25 patients (pts) with coronary artery disease and hypertension (+HTN) and in 25 pts with coronary artery disease only (-HTN). Maximal left main dimensions and left ventricular mass index (LVMI) were measured. +HTN pts had greater LVMI compared to -HTN, (+HTN = 183 +/- 17 g/m2 vs. -HTN = 82 +/- 22 g/m2, p < 0.0001), while maximal left main vessel area was similar (25.99 +/- 5.01 mm2 vs. 25.62 +/- 3.3 mm2, p = 0.8). No correlation was found between LVMI and left main vessel area in + HTN. CONCLUSIONS: Pts with +HTN despite the increased LVMI do not manifest increased LM dimensions. This may affect mid-term clinical outcome.

Adrenergic beta-Antagonists↗
PubMed2003

Consumption of fruits and vegetables in relation to the risk of developing acute coronary syndromes; the CARDIO2000 case-control study.

BACKGROUND: The relation between diet and human health has long been investigated. The aim of this work is to evaluate the association between CHD risk and the consumption of fruit and vegetable, in a large sample of cardiac patients and controls. METHODS: Stratified sampling from all Greek regions, consisted of 848 (700 males, 58 +/- 10 years old and 148 females, 65 +/- 9 years old) randomly selected patients, admitted to the cardiology clinic for a first event of an acute coronary syndrome (ACS). In addition we selected 1078 frequency paired, by sex-age-region, controls in the same hospitals but without any clinical suspicion of CHD. Using validated food-frequency questionnaires we assessed total diet, including fruit and vegetable intake, on a weekly basis. Multiple logistic regression analysis estimated the relative risk of developing ACS by level of fruits and vegetables intake after taking into account the effect of several potential confounders. RESULTS: Data analysis revealed that the benefit of fruit or vegetable consumption increases proportionally by the number of servings consumed (P for trend < 0.001). After adjusting for the conventional cardiovascular risk factors, those in the upper quintile of fruit consumption (5 or more items/day) had 72% lower risk for CHD (odds ratio = 0.28, 95% CI 0.11-0.54, P < 0.001), compared with those in the lowest quintile of intake (< 1 items/day). Similarly, consumption of vegetable more than 3 days/week was associated with 70% lower risk for CHD (odds ratio = 0.30, 95% CI 0.22-0.40, P < 0.001), compared with those that they did not consume vegetables. Of particular interest, a 10% reduction in coronary risk was observed for every one piece of fruit consumed per day (odds ratio = 0.90, 95% CI 0.85-0.97, P = 0.004). CONCLUSIONS: Consumption of fruits and vegetables seems to offer significant protection against CHD.

Journal Article↗
PubMed2003

New balloon-thermography catheter for in vivo temperature measurements in human coronary atherosclerotic plaques: a novel approach for thermography?

Although ex vivo studies showed marked thermal heterogeneity in atheromatic plaques, in in vivo human studies trivial temperature variations are recorded due to the cooling effect of blood flow. We investigated a new balloon-thermogaphy catheter for temperature measurements during coronary flow interruption. A thermistor probe is positioned at the distal segment of the catheter. At the opposite site of the thermistor, a balloon is placed. By inflation of the balloon, coronary flow is interrupted. Ten patients with effort angina were studied. Coronary flow velocity was continuously recorded. Temperature was recorded at the proximal vessel wall and at the lesion before, during, and after complete interruption of blood flow by inflation of the balloon. DeltaTp was assigned as the difference between the background temperature and the maximal temperature during and after balloon inflation. DeltaTl was assigned as the difference between the atherosclerotic plaque and the proximal vessel wall. The procedure was not complicated. DeltaTp during and after balloon inflation was 0.01 +/- 0.01 degrees C and -0.003 +/- -0.01 degrees C (P < 0.001), respectively. DeltaTl was 0.07 +/- 0.04 degrees C at baseline, 0.17 +/- 0.06 degrees C (59.3% +/- 11.8% increase) during, and 0.07 +/- 0.05 degrees C after flow interruption (P < 0.001). DeltaTl was greater than DeltaTp during and after impairment of flow (P < 0.001). In vivo atherosclerotic plaque temperature recording seems to be feasible with this new balloon-thermography catheter. This device may introduce a new approach for the detection of thermal heterogeneity in plaques by addressing the issue of cooling effect of blood flow.

Aged↗