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 ß-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.

Tertiary syphilis and cardiovascular disease: the united triad: case report.

Background: Syphilis, owing to its natural course, can lead to long-term damage to the aortic valve, such as insufficiency and rarely stenosis, ostial coronary stenosis, and syphilitic aortitis. Cardiovascular involvement alongside neurological involvement dominates the prognosis. This should no longer be seen, thanks to awareness and prevention programmes, medical treatment, and antibiotics. Case summary: We report a case of a 54-year-old chronic smoker with no previous history, admitted for respiratory distress amid an impaired general condition. An electrocardiogram was performed, which showed sinus rhythm with lateral ST depression and T-wave inversion. Coronary angiography revealed an ostial stenosis of the left coronary artery. Echocardiography displayed a globular dilated left ventricle with a left ventricular ejection fraction of 40% and severe aortic insufficiency (AI). Computed tomography angiography of the aorta showed a dilation of the thoracic aorta and suprarenal abdominal aorta. Syphilitic serology was positive. The patient underwent angioplasty, resulting in a satisfactory outcome, and subsequently received optimal treatment. Following a consultation with a cardiovascular surgeon and vascular team, it was decided to proceed with mechanical aortic valve replacement and aorto-coronary double bypass surgery, but vascular surgery of the ascending aortic aneurysm was not possible at once. Discussion: Tertiary syphilis should always be considered when faced with isolated coronary ostial involvement, aortic aneurysm, and/or AI. What makes our case special is that the patient had almost all the cardiovascular complications of tertiary syphilis. Primary syphilis should always be prevented, diagnosed early, and treated appropriately with antibiotic therapy.

[Uncommon cause of acute coronary syndrome : Paradoxical embolism]. / Une cause rare de syndrome coronarien aigu : l'embolie paradoxale.

Coronary artery embolism is an uncommon cause of myocardial infarction (MI). Among several etiologies of coronary embolism, we mention a very rare cause which is the paradoxical embolism via patent foramen ovale (PFO). It interests generally youngest people without cardiac risk factors. We report three cases who presented ST-elevation MI (STEMI) due to paradoxical embolism with high risk PFO that can justify embolic infarction. The aim of this article is to define the high risk PFO, to establish causal link between PFO and embolic events and to guide therapeutic management.

L'infarctus du myocarde type 2.

Type 2 MI is a category of myocardial infarction according to the UDMI, frequently encountered in routine practice but still poorly understood in terms of prevalence, diagnostic and therapeutic approach, it affects a heterogeneous population at high risk of major cardiovascular events and non-cardiac death. It is due to an inadequacy between oxygen supply and demand in the absence of a primary coronary event, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension or hypotension. Diagnosis has traditionally required an integrated history assessment, with some combination of indirect evidence of myocardial necrosis based on biochemical, electrocardiographic, and imaging modalities. Differentiation between type 1 and type 2 MI is more complicated than it appears. Treatment of the underlying pathology is the primary goal of treatment.

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

OBJECTIVES: 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).

Cardiac structure and function in Cushing's syndrome: a cardiac magnetic resonance imaging study.

BACKGROUND: Patients with Cushing's syndrome have left ventricular (LV) hypertrophy and dysfunction on echocardiography, but echo-based measurements may have limited accuracy in obese patients. No data are available on right ventricular (RV) and left atrial (LA) size and function in these patients. OBJECTIVES: The objective of the study was to evaluate LV, RV, and LA structure and function in patients with Cushing's syndrome by means of cardiac magnetic resonance, currently the reference modality in assessment of cardiac geometry and function. METHODS: Eighteen patients with active Cushing's syndrome and 18 volunteers matched for age, sex, and body mass index were studied by cardiac magnetic resonance. The imaging was repeated in the patients 6 months (range 2-12 mo) after the treatment of hypercortisolism. RESULTS: Compared with controls, patients with Cushing's syndrome had lower LV, RV, and LA ejection fractions (P < .001 for all) and increased end-diastolic LV segmental thickness (P < .001). Treatment of hypercortisolism was associated with an improvement in ventricular and atrial systolic performance, as reflected by a 15% increase in the LV ejection fraction (P = .029), a 45% increase in the LA ejection fraction (P < .001), and an 11% increase in the RV ejection fraction (P = NS). After treatment, the LV mass index and end-diastolic LV mass to volume ratio decreased by 17% (P < .001) and 10% (P = .002), respectively. None of the patients had late gadolinium myocardial enhancement. CONCLUSION: Cushing's syndrome is associated with subclinical biventricular and LA systolic dysfunctions that are reversible after treatment. Despite skeletal muscle atrophy, Cushing's syndrome patients have an increased LV mass, reversible upon correction of hypercortisolism.