Platelet Inhibition, Endothelial Function, and Clinical Outcome in Patients Presenting With ST-Segment-Elevation Myocardial Infarction Randomized to Ticagrelor Versus Prasugrel Maintenance Therapy: Long-Term Follow-Up of the REDUCE-MVI Trial

Background Off-target properties of ticagrelor might reduce microvascular injury and improve clinical outcome in patients with ST-segment-elevation myocardial infarction. The REDUCE-MVI (Evaluation of Microvascular Injury in Revascularized Patients with ST-Segment-Elevation Myocardial Infarction Treated With Ticagrelor Versus Prasugrel) trial reported no benefit of ticagrelor regarding microvascular function at 1 month. We now present the follow-up data up to 1.5 years. Methods and Results We randomized 110 patients with ST-segment-elevation myocardial infarction to either ticagrelor 90 mg twice daily or prasugrel 10 mg once a day. Platelet inhibition and peripheral endothelial function measurements includi

Incremental prognostic value of hybrid [15O]H2O positron emission tomography-computed tomography: combining myocardial blood flow, coronary stenosis severity, and high-risk plaque morphology

AimsThis study sought to determine the prognostic value of combined functional testing using positron emission tomography (PET) perfusion imaging and anatomical testing using coronary computed tomography angiography (CCTA)-derived stenosis severity and plaque morphology in patients with suspected coronary artery disease (CAD).Methods and resultsIn this retrospective study, 539 patients referred for hybrid [15O]H2O PET-CT imaging because of suspected CAD were investigated. PET was used to determine myocardial blood flow (MBF), whereas CCTA images were evaluated for obstructive stenoses and high-risk plaque (HRP) morphology. Patients were followed up for the occurrence of all-cause death and non-fatal myocardial infarction (MI). During a median follow-up of 6.8 (interquartile range 4.8–7.8) years, 42 (7.8%) patients experienced events, including 23 (4.3%) deaths, and 19 (3.5%) MIs. Annualized event rates for normal vs. abnormal results of PET MBF, CCTA-derived stenosis, and HRP morphology were 0.6 vs. 2.1%, 0.4 vs. 2.1%, and 0.8 vs. 2.8%, respectively (P ConclusionPET-derived MBF, CCTA-derived stenosis severity, and HRP morphology were univariably associated with death and MI, whereas only stenosis severity and HRP morphology provided independent prognostic value.</div

Strain analysis is superior to wall thickening in discriminating between infarcted myocardium with and without microvascular obstruction

Objectives: The aim of the present study was to evaluate the diagnostic performances of strain and wall thickening analysis in discriminating among three types of myocardium after acute myocardial infarction: non-infarcted myocardium, infarcted myocardium without microvascular obstruction (MVO) and infarcted myocardium with MVO. Methods: Seventy-one patients with a successfully treated ST-segment elevation myocardial infarction underwent cardiovascular magnetic resonance imaging at 2-6 days after reperfusion. The imaging protocol included conventional cine imaging, myocardial tissue tagging and late gadolinium enhancement. Regional circumferential and radial strain and associated strain rates were analyzed in a 16-segment model as were the absolute and relative wall thickening. Results: Hyperenhancement was detected in 418 (38%) of 1096 segments and was accompanied by MVO in 145 (35%) of hyperenhanced segments. Wall thickening, circumferential and radial strain were all significantly diminished in segments with hyperenhancement and decreased even further if MVO was also present (all p < 0.001). Peak circumferential strain (CS) surpassed all other strain and wall thickening parameters in its ability to discriminate between hyperenhanced and non-enhanced myocardium (all p < 0.05). Furthermore, CS was superior to both absolute and relative wall thickening in differentiating infarcted segments with MVO from infarcted segments without MVO (p = 0.02 and p = 0.001, respectively). Conclusions: Strain analysis is superior to wall thickening in differentiating between non-infarcted myocardium, infarcted myocardium without MVO and

Hypertension with primary aldosteronism is associated with increased carotid intima-media thickness and endothelial dysfunction

Patients with primary aldosteronism induced hypertension are more likely to experience cardiovascular events compared to patients with essential hypertension. Primary aldosteronism may therefore have distinct adverse effects on cardiovascular structure and function, independent of hypertension. However, current data on such effects of primary aldosteronism are conflicting. The aim of the present study was to investigate the influence of primary aldosteronism on vascular structure and endothelial function, using intima-media thickness as a vascular remodeling index and flow-mediated dilation as a functional parameter. In total, 70 participants were recruited from patients with resistant hypertension. Twenty-nine patients diagnosed with primary aldosteronism and 41 patients with essential hypertension were prospectively enrolled. Primary aldosteronism was due to aldosterone-producing adenoma in 10 cases and due to idiopathic adrenal hyperplasia in 19 cases. All patients underwent ultrasound of the common carotid intima-media thickness and flow-mediated dilation of the brachial artery. Primary aldosteronism patients had significantly lower flow-mediated dilation (3.3 [2.4-7.4] % vs 14.7 [10.3-19.9] %, P  0.05). Hypertensive patients with hyperaldosteronism appear to exhibit deteriorative effects on both vascular structure and function, independent of hypertension

Hypertension with primary aldosteronism is associated with increased carotid intima-media thickness and endothelial dysfunction

Patients with primary aldosteronism induced hypertension are more likely to experience cardiovascular events compared to patients with essential hypertension. Primary aldosteronism may therefore have distinct adverse effects on cardiovascular structure and function, independent of hypertension. However, current data on such effects of primary aldosteronism are conflicting. The aim of the present study was to investigate the influence of primary aldosteronism on vascular structure and endothelial function, using intima-media thickness as a vascular remodeling index and flow-mediated dilation as a functional parameter. In total, 70 participants were recruited from patients with resistant hypertension. Twenty-nine patients diagnosed with primary aldosteronism and 41 patients with essential hypertension were prospectively enrolled. Primary aldosteronism was due to aldosterone-producing adenoma in 10 cases and due to idiopathic adrenal hyperplasia in 19 cases. All patients underwent ultrasound of the common carotid intima-media thickness and flow-mediated dilation of the brachial artery. Primary aldosteronism patients had significantly lower flow-mediated dilation (3.3 [2.4-7.4] % vs 14.7 [10.3-19.9] %, P 0.05). Hypertensive patients with hyperaldosteronism appear to exhibit deteriorative effects on both vascular structure and function, independent of hypertension

Hypertension with primary aldosteronism is associated with increased carotid intima‐media thickness and endothelial dysfunction

Patients with primary aldosteronism induced hypertension are more likely to experience cardiovascular events compared to patients with essential hypertension. Primary aldosteronism may therefore have distinct adverse effects on cardiovascular structure and function, independent of hypertension. However, current data on such effects of primary aldosteronism are conflicting. The aim of the present study was to investigate the influence of primary aldosteronism on vascular structure and endothelial function, using intima-media thickness as a vascular remodeling index and flow-mediated dilation as a functional parameter. In total, 70 participants were recruited from patients with resistant hypertension. Twenty-nine patients diagnosed with primary aldosteronism and 41 patients with essential hypertension were prospectively enrolled. Primary aldosteronism was due to aldosterone-producing adenoma in 10 cases and due to idiopathic adrenal hyperplasia in 19 cases. All patients underwent ultrasound of the common carotid intima-media thickness and flow-mediated dilation of the brachial artery. Primary aldosteronism patients had significantly lower flow-mediated dilation (3.3 [2.4-7.4] % vs 14.7 [10.3-19.9] %, P  0.05). Hypertensive patients with hyperaldosteronism appear to exhibit deteriorative effects on both vascular structure and function, independent of hypertension