Anévrysme ventriculaire gauche et communication interventriculaire compliquant un infarctus du myocarde

L'association d'une communication interventriculaire post infarctus du myocarde et d'un anévrysme du  ventricule gauche chez un même patient est extrêmement rare et survient habituellement durant la première semaine qui suit un infarctus du myocarde. Nous rapportons le cas insolite d'un patient âgé de 63 ans, admis pour choc cardiogénique en rapport avec une communication inter ventriculaire apicale et un anévrysme  ventriculaire gauche causés par un infarctus du myocarde antérieur. La correction chirurgicale a consisté en une fermeture du défect septal par un patch en dacron via une ventriculotomie gauche associée à une  anévrysectomie et un mono pontage coronaire. Cette observation illustre d'une part la rareté de l'association communication inter ventriculaire-anévrysme ventriculaire gauche post infarctus du myocarde, et d'autre part l'efficacité du traitement chirurgical qui reste la seule option salvatrice pour cette pathologie. Key words: Infarctus du myocarde, anévrysme ventriculaire gauche, communication inter ventriculair

Stable angina revealing a post-traumatic coronary cameral fistula: A case report

Coronary-cameral fistulas are abnormal connections between coronary arteries and any of the heart chambers, It may be acquired or congenital (whether isolated or along with congenital heart diseases); It is usually asymptomatic in younger patients; but with increasing age, symptoms begin to appear, and the incidence of complication rises. Coronary angiography is the gold standard in diagnosis but echography and cardiac magnetic resonance imaging may be also useful. It can be treated medically with β-blockers or calcium channel blockers, but large fistulas with hemodynamic significant shunts should be closed by transcatheter or surgical means. We present a 57-year-old patient with a history of chest trauma, that present fistulas connecting the 3 coronary arteries to the left ventricle chamber complicated by myocardial ischemia causing stable angina

Aldosterone-Related Myocardial Extracellular Matrix Expansion in Hypertension in Humans A Proof-of-Concept Study by Cardiac Magnetic Resonance

International audienceObjectives: This study sought to assess the respective effects of aldosterone and blood pressure (BP) levels on myocardial fibrosis in humans.Background: Experimentally, aldosterone promotes left ventricular (LV) hypertrophy, and interstitial myocardial fibrosis in the presence of high salt intake.Methods: The study included 20 patients with primary aldosteronism (PA) (high aldosterone and high BP), 20 patients with essential hypertension (HTN) (average aldosterone and high BP), 20 patients with secondary aldosteronism due to Bartter/Gitelman (BG) syndrome (high aldosterone and normal BP), and 20 healthy subjects (HS) (normal aldosterone and normal BP). Participants in each group were of similar age and sex distributions, and asymptomatic. Cardiac magnetic resonance including cine and T1 mapping was performed blind to the study group to quantify global LV mass index, as well as intracellular mass index and extracellular mass index considered as a measure of myocardial fibrosis in vivo.Results: Median plasma aldosterone concentration was as follows: PA = 709 pmol/l (interquartile range [IQR]: 430 to 918 pmol/l); HTN = 197 pmol/l (IQR: 121 to 345 pmol/l); BG = 297 pmol/l (IQR: 180 to 428 pmol/l); and HS = 105 pmol/l (IQR: 85 to 227 pmol/l). Systolic BP was as follows: PA = 147 ± 15 mm Hg; HTN = 133 ± 19 mm Hg; BG = 116 ± 9 mm Hg; and HS = 117 ± 12 mm Hg. LV end-diastolic volume showed underloading in BG and overloading in patients with PA (63 ± 13 ml/m2 vs. 82 ± 15 ml/m2; p < 0.0001). Intracellular mass index increased with BP across groups (BG: 36 [IQR: 29 to 41]; HS: 40 [IQR: 36 to 46]; HTN: 51 [IQR: 42 to 54]; PA: 50 [IQR: 46 to 67]; p < 0.0001). Extracellular mass index was similar in BG, HS, and HTN (16 [IQR: 12 to 20]; 15 [IQR: 11 to 18]; and 14 [IQR: 12 to 17], respectively) but 30% higher in PA (21 [IQR: 18 to 29]; p < 0.0001) remaining significant after adjustment for mean BP.Conclusions: Only primary pathological aldosterone excess combined with high BP increased both extracellular myocardial matrix and intracellular mass. Secondary aldosterone excess with normal BP did not affect extracellular myocardial matrix. (Study of Myocardial Interstitial Fibrosis in Hyperaldosteronism; NCT02938910)