Maria Drakopoulou

Detection of Luminal-Intimal Border and Coronary Wall Enhancement in Intravascular Ultrasound Imaging After Injection of Microbubbles and Simultaneous Sonication With Transthoracic Echocardiography

A 61-year-old man presented with unstable angina (Braunwald class 2B). Coronary angiography revealed a mild lesion on the very proximal segment of the left anterior descending coronary artery (LAD) and a significant stenosis (80%) in the mid-segment. Intracoronary ultrasound was used to further evaluate proximal coronary artery stenosis. It was found to be a soft plaque without significant luminal stenosis but without clear definition of the luminal-intimal boundary. Intravenous injection of gas-filled microbubble ultrasound contrast agents have been used for endocardial border detection, especially when they are sonicated by acoustic power and …

Incremental Predictive Value of Carotid Inflammation in Acute Ischemic Stroke

Background and Purpose— Microwave Radiometry (MWR) allows in vivo noninvasive assessment of internal temperature of tissues. The aim of the present study was to evaluate in patients with ischemic stroke and bilateral carotid plaques (1) whether ipsilateral carotid arteries exhibit higher temperature differences (&Dgr;T), as assessed by MWR; (2) the predictive accuracy of MWR in symptomatic carotid artery identification. Methods— Consecutive patients with recent acute anterior circulation ischemic stroke because of large artery atherosclerosis were included in the study. Carotid arteries of all patients were evaluated by carotid ultrasound and MWR. Results— In total, 50 patients were included in the study. Culprit carotid arteries had higher &Dgr;T compared with nonculprit (0.93±0.58 versus 0.58±0.35°C; P<0.001). The addition of &Dgr;T to a risk prediction model based only on ultrasound plaque characteristics increased its predictive accuracy significantly (c-statistic: 0.691 versus 0.768; Pdif=0.05). Conclusions— Culprit carotid arteries show higher thermal heterogeneity compared with nonculprit carotid arteries in patients with acute ischemic stroke and bilateral carotid plaques. MWR has incremental value in culprit carotid artery discrimination.

Association of inflammatory markers with angiographic severity and extent of coronary artery disease

Inflammatory processes play a pivotal role in the pathogenesis of atherosclerosis and mediate many of the stages of atheroma development, from initial leukocyte recruitment to eventual rupture of the unstable atherosclerotic plaque. Several systemic inflammatory markers reflect different degrees of inflammation and have been indicated as independent risk factors in cardiovascular disease, especially in unstable coronary syndromes. However, whether elevated levels of circulating inflammatory markers play a role in the extent and severity of atherosclerosis remains controversial. The present review summarizes our current understanding of the relationship between inflammatory markers and the presence and extent of coronary atherosclerosis, in order to assess the potential utility of these markers in identifying patients with higher levels of atherosclerotic burden.

New insights by optical coherence tomography into the differences and similarities of culprit ruptured plaque morphology in non-ST-elevation myocardial infarction and ST-elevation myocardial infarction.

BACKGROUND Plaque rupture is the most common pathology associated with non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI). However, limited data are available regarding ruptured plaque morphology and its relationship with the clinical syndrome. This study aimed (1) to provide a morphologic description of ruptured culprit lesions by optical coherence tomography (OCT) and (2) to investigate whether ruptured plaque morphology differs between NSTEMI and STEMI. METHODS We included 84 consecutive patients with NSTEMI and STEMI undergoing OCT study of the culprit lesion. We identified patients with plaque rupture in the OCT study and used them as the study population. Qualitative and quantitative analysis of ruptured plaque morphology was then performed, followed by a comparison of the morphological characteristics in patients with STEMI and NSTEMI. RESULTS Fifty-five patients (70.5%) with rupture, 25 with NSTEMI, and 30 with STEMI were used for analysis. Plaque was ruptured at the minimal lumen in 34.5% of the cases, whereas 69% of the ruptures occurred at the plaque shoulder. Ruptured cap thickness was ≤90 μm in 96% of ruptured plaques. Patients with NSTEMI had greater minimal luminal area (P < .001), less lipid content (P = .01), and lower rupture length (P < .001) and length of missing fibrous cap (P < .05) compared with patients with STEMI. CONCLUSIONS Rupture of the plaque in myocardial infarction usually occurs in sites different than the minimal lumen and at the shoulder of areas with fibrous cap measuring ≤90 μm. Patients with STEMI have greater plaque disruption and smaller minimal lumen area than patients with NSTEMI.

First In Vivo Application of Microwave Radiometry in Human Carotids: A New Noninvasive Method for Detection of Local Inflammatory Activation

OBJECTIVES This study investigated whether temperature differences: 1) can be measured in vivo noninvasively by microwave radiometry (MR); and 2) are associated with ultrasound and histological findings. BACKGROUND Studies of human carotid artery samples showed increased heat production. MR allows in vivo noninvasive measurement of internal temperature of tissues. METHODS Thirty-four patients undergoing carotid endarterectomy underwent screening of carotid atherosclerosis by ultrasound and MR. Healthy volunteers were enrolled as a control group. During ultrasound study, plaque texture, plaque surface, and plaque echogenicity were analyzed. Temperature difference (ΔT) was assigned as maximal minus minimum temperature. Association of thermographic with ultrasound and histological findings was performed. RESULTS ΔT was higher in atherosclerotic carotid arteries compared with the carotid arteries of controls (p < 0.01). Fatty plaques had higher ΔT compared with mixed and calcified (p < 0.01) plaques. Plaques with ulcerated surface had higher ΔT compared with plaques with irregular and regular surface (p < 0.01). Heterogeneous plaques had higher ΔT compared with homogenous (p < 0.01). Specimens with thin fibrous cap and intense expression of CD3, CD68, and vascular endothelial growth factor (VEGF) had higher ΔT compared with specimens with thick cap and low expression of CD3, CD68, and VEGF (p < 0.01). CONCLUSIONS MR provides in vivo noninvasive temperature measurements of carotid plaques, reflecting plaque inflammatory activation.

Vulnerable plaque and inflammation: potential clinical strategies.

Although enormous progress has been made in the prevention and treatment of cardiovascular disease, it still remains the leading cause of death worldwide. During the last decades, advances in the understanding of the pathophysiology of vulnerable plaque progression, coupled with novel diagnostic and therapeutic approaches, created a new opportunity for progress against cardiovascular disease. It has been demonstrated that inflammation, implicated in all stages of atherosclerosis, is an integral part of vulnerable plaque development and progression, leading eventually to plaque instability. Thus, new diagnostic modalities have been proposed for the detection of local plaque inflammation. Moreover, treatments such as stenting, photodynamic therapy, and novel pharmaceutical agents are under consideration as methods to stabilize the vulnerable plaques by inhibiting inflammation. This review provides an overview of the inflammatory process leading to atherosclerotic cardiovascular disease and the potential clinical strategies that may substantially decrease the incidence of events. We will mention the major impact of local and systemic inflammation on plaque advancing and destabilization, the imaging techniques for early detection of vulnerable plaques and the potential therapeutic strategies.

Advancing therapy for hypercholesterolemia

Importance of the field: Hypercholesterolemia holds a key role in the development and progression of atherosclerosis and is a causative factor of coronary artery disease. Current guidelines for cholesterol treatment target low-density cholesterol (LDL-C) as the primary goal of therapy. Despite advances in the pharmacotherapy of atherosclerosis, the most successful agents used to treat this disease – HMG CoA reductase inhibitors – remain ineffective for the primary or secondary prevention of myocardial infarction in 50 – 60% of patients. Advancing therapy for hypercholesterolemia with new-emerging drugs either as monotherapy or in combination will hopefully improve cardiovascular outcomes. Areas covered in this review: The two major sources of cholesterol in the human body are: i) biosynthesis of cholesterol by the liver; and ii) absorption by the intestines. Both play a pivotal role in the overall balance of cholesterol. A recent and more effective therapeutic strategy is to treat both sources of cholesterol simultaneously with a complementary mechanism of action. The present article presents cholesterol metabolism and reviews new emerging lipid-lowering drugs and therapies that: i) lower LDL-C; ii) lower triglycerides; and iii) increase high-density lipoprotein cholesterol. What the reader will gain: This review summarizes the pivotal role of both the liver and intestine in the overall balance of cholesterol in the body and describe the clinical impact and relevance of using new emerging lipid-lowering drugs either alone or co-administered with statins in controlling cholesterol levels. Take-home message: An elevated concentration of LDL-C plays a causal role in the development of cardiovascular disease. The new aggressive cholesterol treatment goals call for a more advanced therapeutic approach to maximize the cardiovascular benefits associated with lower LDL-C levels.

A new non-invasive method for detection of local inflammation in atherosclerotic plaques: experimental application of microwave radiometry.

Inflammation is implicated in theprogression and the instability f atheromatic plaques [1–9]. Previous studies have demonstrated hat local inflammatory activation is correlated with the temperture of the atheromatic plaques [1,2,5,10–12,8]. For the in vivo ssessment of plaque inflammatory activation intravascular therography (IVT) has been applied with dedicated intravascular atheters [2,8,10,12,13,14]. Indeed, IVT is an invasive method, hichprovides additional diagnostic andprognostic information in he identification of the high-risk atheromatic plaques in patients ith coronary artery disease [3,5,9,10,13]. Although IVT has diagnostic and prognostic implications, there re several limitations of current technology limiting its clinical use 13,15,16]. The invasive approachof themethodexcludes the appliation of IVT in primary prevention. Moreover, as there are several echnical shortcomings of the available intravascular catheters, a rospective study with distinct endpoints cannot be performed. hus, the evaluation of the diagnostic and prognostic implications f IVT is infeasible with the current technology.

Morphological Characteristics of Culprit Atheromatic Plaque Are Associated With Coronary Flow After Thrombolytic Therapy: New Implications of Optical Coherence Tomography From a Multicenter Study

OBJECTIVES This study investigated the association between morphological characteristics of culprit atheromatic lesions as assessed by optical coherence tomography and Thrombolysis In Myocardial Infarction (TIMI) flow grade after thrombolysis in patients with ST-segment elevation myocardial infarction (STEMI). BACKGROUND Although several variables have been found to predict coronary flow after thrombolysis in patients with STEMI, the impact of culprit lesion morphology has not been studied. METHODS Fifty-five patients with STEMI from 3 tertiary centers that were treated with thrombolysis and underwent optical coherence tomography examination in the culprit lesion between 24 and 48 h after thrombolysis were included in the study. Patients were categorized on the basis of TIMI flow grade into patients with TIMI flow grade 3 versus TIMI flow grade < or =2. RESULTS Patients with TIMI flow grade < or =2 had plaques with more lipid quadrants than patients with TIMI flow grade 3 (p < 0.001), and presented with greater incidence of plaque rupture (p = 0.001). Mean minimal cap thickness was greater in patients with patent arteries than in patients with impaired flow (87 +/- 26 microm vs. 48 +/- 18 microm, p < 0.0001). Minimal cap thickness was independently associated with TIMI flow grade. CONCLUSIONS The morphological characteristics of the culprit atheromatic lesion in patients with STEMI are associated with coronary flow after thrombolysis. The lipid content, the existence of rupture, and mainly the thickness of the fibrous cap are associated with the outcome of thrombolysis.

In Vivo Aortic Valve Thermal Heterogeneity in Patients With Nonrheumatic Aortic Valve Stenosis: The First In Vivo Experience in Humans

OBJECTIVES We investigated in vivo in aortic valve stenosis (AVS) whether there is: 1) thermal heterogeneity within the valve leaflets; 2) temperature difference between the leaflets and the ascending aortic wall; and 3) a possible correlation between heat production, inflammation, and neoangiogenesis. BACKGROUND Histological studies have demonstrated a potential role of inflammation and neoangiogenesis in AVS. METHODS We examined 96 leaflets scheduled for aortic valve replacement. Twenty-five patients had AVS, and 7 had aortic valve insufficiency (AVI). Temperature measurements were performed right before hypothermic cardioplegia. Temperature difference (DeltaT) was assigned as the mean temperature of each leaflet minus the temperature of the aortic wall. Histological, immunohistological analysis, and vascular endothelial growth factor (VEGF) immunoreactivity was performed. RESULTS Significant thermal heterogeneity was recorded within the leaflets of AVS, compared with AVI (1.52 +/- 1.35 degrees C vs. 0.13 +/- 0.11 degrees C, p < 0.01). In AVS DeltaT was greater in all leaflets compared with the AVI group (p < 0.01). Leaflets of AVS had increased inflammatory cell infiltration, calcium deposit, and anti-VEGF expression compared with AVI (p < 0.01). CONCLUSIONS Thermal heterogeneity is increased in AVS and correlates with inflammatory mononuclear cell infiltration, expression of pro-inflammatory cytokines and neoangiogenic factors.