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Biomedical subjects

Maria Drakopoulou

Publications and source records attributed to Maria Drakopoulou.

8 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

Coronary sinus thermography in idiopathic dilated cardiomyopathy: correlation with systemic inflammation and left ventricular contractility.

BACKGROUND: Previous studies have demonstrated that patients with heart failure have increased myocardial heat production. Coronary sinus (CS) thermography is a new method for the evaluation of left ventricular heat production. AIMS: We investigated whether the CS blood temperature is increased in patients with idiopathic dilated cardiomyopathy (DCM) compared to a control group and whether the CS blood temperature correlates with ejection fraction and systemic inflammatory activation. METHODS AND RESULTS: We included 25 patients with DCM and 22 healthy subjects. Temperature measurements were performed using a new thermography catheter. Temperature difference (DeltaT) was defined as the difference between the CS and RA blood temperature. The CRP levels were also measured. DeltaT was significantly greater in patients with DCM compared to the controls (0.25+/-0.09 vs 0.14+/-0.07 degrees C, p<0.01). DeltaT and EF were inversely correlated in patients with DCM (R=0.43). We categorized patients with DCM into two groups using a CRP cut-off value of < or =1 mg/dL. DeltaT in patients with high CRP was less (0.21+/-0.06 degrees C) compared to patients with low CRP (0.30+/-0.08 degrees C, p=0.01). CONCLUSIONS: In patients with DCM increased heat production from the myocardium, as estimated from the coronary sinus blood temperature, was demonstrated, interestingly there was no correlation with systemic inflammatory activation.

Body Temperature↗
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

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↗
PubMed2005

Intracoronary thermography: does it help us in clinical decision making?

The concept of the "vulnerable" plaque has recently emerged to explain how quiescent atherosclerotic lesions evolve to cause clinical events. The morphologic and immunologic determinants specific for the vulnerable plaque have been reported: a large lipid core (>or=40% plaque volume) composed of free cholesterol crystals, cholesterol esters, and oxidized lipids impregnated with tissue factor; a thin fibrous cap depleted of smooth muscle cells and collagen; an outward (positive) remodeling; inflammatory cell infiltration of fibrous cap and adventitia (mostly monocyte-macrophages, some activated T cells, and mast cells); and increased neovascularity. Despite the large amount of information regarding the morphological characteristics of remote lesions, we lack studies with functional assessment of non-culprit lesions. Coronary thermography is a technique for functional assessment of coronary atherosclerotic plaques. Several catheter designs have been proposed. There are catheters with thermistor(s) and wires with thermal sensors at the distal tip. All designs have several advantages and disadvantages. Despite the current limitations of coronary thermography, we gained important pathophysiological and clinical information regarding the vulnerability of atheromatic plaques. It has been documented both experimentally and clinically that increased heat generation is associated with increased macrophage concentration within the plaque. The correlation between local inflammatory involvement and local heat generation has also been observed with the peripheral inflammatory markers such as C-reactive protein. Whether systemic treatment, with agents such as statins or interventional techniques, such as drug-eluting stents, will have an impact on stabilizing vulnerable plaques need to be determined in future studies. In conclusion, although there are several techniques for evaluating morphologically atheromatic plaques, thermography is a promising method for the functional assessment of vulnerable plaque and has been introduced into clinical practice, with a good predictive value for clinical events in patients with increased temperature in the atherosclerotic plaque.

Coronary Artery Disease↗
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↗
PubMedDate not supplied

Patients with type two diabetes mellitus: increased local inflammatory activation in culprit atheromatous plaques.

INTRODUCTION: Diabetes mellitus (DM) predisposes to coronary artery disease (CAD). The progression of CAD has recently come to be regarded as an inflammatory activation. Thermography detects local inflammatory involvement as heat generation. The aim of this study was to investigate whether patients with CAD and DM have increased local heat generation compared to non-diabetic patients. METHODS: We enrolled 45 patients with DM and 63 non-diabetic patients who were undergoing percutaneous coronary interventions. The two groups were matched for age, type of clinical syndrome, statin and aspirin intake and angiographic stenosis (%). Coronary thermography was performed and the temperature difference (deltaT) between the atherosclerotic plaque and the proximal vessel wall was measured. RESULTS: Patients with DM had increased deltaT compared to non-diabetic patients (deltaT: 0.17 +/- 0.18 degrees C vs. 0.09 +/- 0.02 degrees C, p = 0.01). Patients with DM and acute coronary syndromes (ACS)(n=21) had increased deltaT compared to non-diabetic patients (n=22) (deltaT: 0.29 +/- 0.31 degrees C vs. 0.15 +/- 0.21 degrees C, p = 0.02). Similarly, patients with DM and stable angina (SA) had a higher deltaT than non-diabetics with SA (deltaT: 0.09 +/- 0.08 degrees C vs. 0.05 +/- 0.04 degrees C, p = 0.006). CONCLUSION: Patients with DM have increased deltaT compared to non-diabetic patients.

Aged↗