Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to disseminate knowledge & skills of Acute Cardiovascular Care.
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our mission is to promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
The ESC Councils' goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Renata Cifkova ,
New techniques for the Evaluation of Hypertensive Heart Disease Petros Nihoyannopoulos, London, UK
Comprehensive two-dimensional and Doppler echocardiography can assess abnormal relaxation, detect changes in compliance or stiffness, and differentiate the level of filling pressure from the rate of change in pressure during diastole, which together with the structural information obtained from the two-dimensional echocardiography provides a clinically relevant assessment of diastolic function. By demonstrating intrinsic diastolic dysfunction in patients with clinical evidence of heart failure and normal EF, echocardiography can diagnose diastolic heart failure reliably using speckle tracking and deformation techniques. Diastolic dysfunction may be related to diffuse myocardial fibrosis through interstitial collagen infiltration, which is difficult to visualize by any imaging modality, but also as a result of arterial stiffness and reduced arterial compliance.
Coronary Flow in Hypertension Enrico Agabiti-Rosei, Brescia, Italy Hypertension is often associated with myocardial ischemia and with clinical manifestations of coronary heart disease (CHD). In fact, hypertension may lead to reduced coronary reserve (CFR) as a consequence of the development of 1) coronary atherosclerotic plaques, 2) structural and functional alteration of microcirculation, 3) left ventricular hypertrophy. In addition, myocardial oxygen demand is frequently increased in hypertension. A decrease of myocardial blood flow (MBF) or of CFR, in the absence of angiographically demonstrable stenosis of the epicardial coronary arteries, indicates an impairment of coronary microcirculation. CFR may be evaluated at maximal vasodilatation by measuring LAD coronary artery flow (echo) or, more precisely, MBF using Positron Emission Tomography (PET). Reducing BP prevents CHD, but too low or too rapid decrease of BP may even be dangerous in patients with clinically evident cardiovascular damage. Some drugs, such as calcium antagonists and those inhibiting the renin angiotensin system, seem more effective in preventing or reversing abnormalities of microcirculation. Technical progress may permit in the future an easier measurement of MBF, thus providing an important end-point for the assessment of the efficacy of antihypertensive treatment.
Blood vessels in hypertension: an update on carotid intima-media thickness and arterial stiffness measurement Stephane Laurent, Paris, France
The 2007 ESH-ESC guidelines classify patients with subclinical organ damage as individuals with high added risk. Carotid wall thickening and plaques are considered markers of atherosclerosis, and they are related to intimal changes, whereas aortic stiffness is a marker of arteriosclerosis, related to changes within the media of the arterial wall. Aortic pulse wave velocity (PWV) increases with age and is higher in hypertensive individuals. Carotid-femoral PWV is currently considered the gold standard for measurement of aortic stiffness. A meta-analysis of 17 studies (Vlachopoulos et al., JACC 2010) showed that carotid-femoral PWV has a predictive value for all-cause and CV mortality and CV morbidity. Several studies confirmed that PWV adds predictive value to standard prediction of events by conventional risk stratification (SCORE, ESH risk chart, Framingham risk). A meta-analysis of 16 studies by Lorenz et al. (Lancet 2012) has shown that increased intima-media thickness (IMT) is associated with increased hazard ratio for myocardial infarction, stroke and CV death. In the ARIC Study, carotid IMT and presence of plaque improved the prediction of primary CHD. The level of evidence is lower if IMT is measured by conventional imaging systems. Therefore, carotid IMT should be accurately measured using high resolution echo-tracking systems(ET-IMT). Carotid IMT may not be useful for the risk stratification of individuals in the general population. PWV and ET-IMT should be measured in outcome trials to demonstrate that they are true surrogate endpoints. How far should blood pressure be lowered in high-risk patients? Josep Redon, Valencia, Spain
Guidelines have recommended more aggressive antihypertensive treatment in diabetes and high-risk patients, aiming at values <130 mmHg systolic and 80 mmHg diastolic. However, the additional beneficial effects of such lower BP targets remain unproven. The results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study showed that, in patients with type 2 diabetes, targeting at SBP to <120 mm Hg did not reduce the rate of CV events, compared to subjects in whom the SBP target was < 140 mmHg, except for stroke. Likewise, a post-hoc analysis of the International Verapamil SR-Trandolapril Study (INVEST) concluded that reducing SBP to <130 mmHg in patients with diabetes and coronary artery disease was not associated with improved CV outcomes compared with usual BP control. In these studies, as well as in the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET), the relationship of initial or in-treatment SBP with myocardial infarction or CV mortality was different from that for stroke because the risk of either event was not significantly related to the baseline SBP value and was flat over a wide range of in-treatment values. Antihypertensive treatment should be expected to exert a clear-cut protective effect against macrovascular complications when initial SBP values are high. At lower initial SBP, in the 130-142 mmHg range, the benefit of BP reduction originates mainly from protection against stroke. Finally, around or below an initial SBP of 130 mmHg, antihypertensive treatment should be instituted with caution because of the possibility of untoward cardiac effects that could counterbalance the beneficial consequences of aggressive BP reduction for stroke. In this case, identification of the frail patient at high risk for coronary events should be encouraged in prospective studies.
Hypertension and the heart
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