Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction.

To investigate the influence of cardiovascular magnetic resonance (CMR) timing after reperfusion on CMR-derived parameters of ischemia/reperfusion (I/R) injury in patients with ST-segment elevation myocardial infarction (STEMI). The study included 163 reperfused STEMI patients undergoing CMR during the index hospitalization. Patients were divided according to the time between revascularization and CMR (T <sub>revasc-CMR</sub> : Tertile-1 ≤ 43; 43 < Tertile-2 ≤ 93; Tertile-3 > 93 h). T2-mapping derived area-at-risk (AAR) and intramyocardial-hemorrhage (IMH), and late gadolinium enhancement (LGE)-derived infarct size (IS) and microvascular obstruction (MVO) were quantified. T1-mapping was performed before and > 15 min after Gd-based contrast-agent administration yielding extracellular volume (ECV) of infarct. Main factors influencing I/R injury were homogenously balanced across T <sub>revasc-CMR</sub> tertiles. T2 values of infarct and remote regions increased with increasing T <sub>revasc-CMR</sub> tertiles (infarct: 60.0 ± 4.9 vs 63.5 ± 5.6 vs 64.8 ± 7.5 ms; P < 0.001; remote: 44.3 ± 2.8 vs 46.1 ± 2.8 vs ± 46.1 ± 3.0; P = 0.001). However, T2 value of infarct largely and significantly exceeded that of remote myocardium in each tertile yielding comparable T2-mapping-derived AAR extent throughout T <sub>revasc-CMR</sub> tertiles (17 ± 9% vs 19 ± 9% vs 18 ± 8% of LV, respectively, P = 0.385). Similarly, T2-mapping-based IMH detection and quantification were independent of T <sub>revasc-CMR</sub> . LGE-derived IS and MVO were not influenced by T <sub>revasc-CMR</sub> (IS: 12 ± 9% vs 12 ± 9% vs 14 ± 9% of LV, respectively, P = 0.646). In 68 patients without MVO, T1-mapping based ECV of infarct region was comparable across T <sub>revasc-CMR</sub> tertiles (P = 0.470). In STEMI patients, T2 values of infarct and remote myocardium increase with increasing CMR time after revascularization. However, these changes do not give rise to substantial variation of T2-mapping-derived AAR size nor of other CMR-based parameters of I/R. ISRCTN03522116 . Registered 30.4.2018 (retrospectively registered)

Association of the PHACTR1/EDN1 genetic locus with spontaneous coronary artery dissection

Background: Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndromes (ACS) afflicting predominantly younger to middle-aged women. Observational studies have reported a high prevalence of extracoronary vascular anomalies, especially fibromuscular dysplasia (FMD) and a low prevalence of coincidental cases of atherosclerosis. PHACTR1/EDN1 is a genetic risk locus for several vascular diseases, including FMD and coronary artery disease, with the putative causal noncoding variant at the rs9349379 locus acting as a potential enhancer for the endothelin-1 (EDN1) gene. Objectives: This study sought to test the association between the rs9349379 genotype and SCAD. Methods: Results from case control studies from France, United Kingdom, United States, and Australia were analyzed to test the association with SCAD risk, including age at first event, pregnancy-associated SCAD (P-SCAD), and recurrent SCAD. Results: The previously reported risk allele for FMD (rs9349379-A) was associated with a higher risk of SCAD in all studies. In a meta-analysis of 1,055 SCAD patients and 7,190 controls, the odds ratio (OR) was 1.67 (95% confidence interval [CI]: 1.50 to 1.86) per copy of rs9349379-A. In a subset of 491 SCAD patients, the OR estimate was found to be higher for the association with SCAD in patients without FMD (OR: 1.89; 95% CI: 1.53 to 2.33) than in SCAD cases with FMD (OR: 1.60; 95% CI: 1.28 to 1.99). There was no effect of genotype on age at first event, P-SCAD, or recurrence. Conclusions: The first genetic risk factor for SCAD was identified in the largest study conducted to date for this condition. This genetic link may contribute to the clinical overlap between SCAD and FMD

Spontaneous dissecting coronary haematoma with and without intimal tear

International audienc

Association Between Protein Intake and Mortality in Hypertensive Patients Without Chronic Kidney Disease in the OLD-HTA Cohort

International audienceProtein intake may have some benefits on reducing blood pressure and cardiovascular events, but their effects are still debated. The objective of this study was to test the prognostic value of protein intake assessed by 24-hour urinary urea in a cohort of hypertensive patients with preserved renal function. A total of 1128 hypertensive patients were followed according to tertile of protein intake adjusted for ideal body weight: \textless0.70, 0.70 to 0.93, and \textgreater0.93 g/kg. Baseline characteristics (mean+/-standard deviation) were age 45.1+/-13.2 years, systolic/diastolic blood pressure 185+/-32/107+/-20 mm Hg, and estimated glomerular filtration rate 82+/-32 mL/min. After 10 years of follow-up, 289 deaths occurred, 202 of which were of cardiovascular cause. After adjustment for major cardiovascular risk factors, patients in the second and third tertiles of protein intake had a decreased risk of all-cause death (hazard ratio [95% confidence interval], 0.71 [0.56-0.91]) and cardiovascular death (0.72 [0.54-0.96]), but not of stroke death (0.72 [0.41-1.28]) in comparison to patients in the low protein intake tertile. Normal-high protein intake was associated with a better outcome in a subset of the population: younger patients, low salt intake, without aortic atherosclerosis, or previous cardiovascular events (Pinteraction\textless0.10 for all). Hypertensive patients having a protein intake \textgreater0.7 g/kg ideal body weight, particularly those at low risk, had lower all-cause and cardiovascular mortality rates. Physicians may encourage hyper tensive patients to have normal or high protein diet in addition to low salt consumption, moderate alcohol consumption, and regular physical activity

Screening for hypertension-mediated organ damage and aetiology: still of value after 65 years of age?

International audienceBACKGROUND: Secondary forms and hypertension-mediated organ damage (HMOD) may differ between younger and older hypertensive patients. The aim of the present study was to explore the specificity of HMOD and secondary forms in patients ≥ 65 years in comparison to younger ones in a contemporary cohort. METHODS: We analysed 938 patients recruited between 2004 and 2014 (Cardiology department, Croix-Rousse Hospital, Lyon) who had at baseline HMOD and secondary forms screening among them 190 were ≥ 65 years. RESULTS: The mean (2.1 ± 0.8 vs. 1.2 ± 0.9, P \textless 0.001) and frequency of HMOD (96.3% vs. 72.9%, P \textless 0.001) was higher in patients ≥ 65 years than younger ones. Carotid femoral pulse wave velocity \textgreater 10 m/s was the most frequent HMOD in patients ≥ 65 years (90.1%), while echocardiographic left ventricular hypertrophy was the most common in the younger patients (45.0%). Among ECG left ventricular indexes, only R wave in aVL lead was significantly more frequently observed in patients ≥ 65 years (32.6%) than in younger ones (19.0%, P \textless 0.001). The frequency of secondary hypertension was not significantly different between younger and older patients (respectively; 30.5% vs. 27.8%, P = 0.487). The most frequent aetiology was primary aldosteronism regardless of age, followed by renovascular hypertension (6.3% vs. 3.3%, P = 0.038). Among older patients, 3.2% were treated with adrenalectomy and 6.3% with percutaneous transluminal renal angioplasty. CONCLUSION: Extensive screening of HMOD in older patients may be questionable as nearly all patients had one; aetiology must however be explored as a third of older patients had a secondary form