Incidental detection of myocardial clefts in a patient with acute inferior ST-segment elevation myocardial infarction: a very unusual and potentially ominous association-a case-report.

BACKGROUND: The crescent availability of high-resolution cardiac imaging allows detection of myocardial structural variations. Differentiate these entities from others with different clinical significance can be challenging. Clinicians should be familiar with myocardial clefts to avoid erroneous diagnosis. CASE SUMMARY: A 63-year-old smoker man alerted the emergency medical system for sudden chest pain. The electrocardiogram showed Pardee wave in inferior leads. Coronary angiography evidenced a 100% occlusion of right coronary artery that was treated by angioplasty and drug-eluting stent implantation with optimal angiographic result. At ventriculography, two fissure-like protrusion were observed in the inferior wall. Urgent transthoracic echocardiogram (TTE) demonstrated two deep fissures on the mid-inferior wall, contained by a thin sub-epicardial layer, with sub-total obliteration during systole. A diagnosis of myocardial clefts was suspected and after Heart Team discussion, a conservative strategy was proposed. Early cardiac magnetic resonance (CMR) confirmed two myocardial crypts on the mid-inferior wall. Stability of myocardial fissures and absence of left ventricular remodelling was confirmed by TTE, in a 2 years of follow-up period. DISCUSSION: Myocardial cleft should always be considered in the differential diagnosis of myocardial wall defects. In a patient presenting with an acute myocardial infarction, the main differential diagnosis is pseudoaneurysm. In this setting modified TTE views and meticulous analysis of CMR sequences are recommended to confirm the diagnosis and estimate the risk of myocardial rupture.

Sudden cardiogenic shock mimicking fulminant myocarditis in a surviving teenager affected by severe acute respiratory syndrome coronavirus 2 infection.

In the context of the coronavirus disease 2019 pandemic, myocardial injury is a relatively frequent finding. Progression to cardiogenic shock has been rarely described, especially in healthy young patients. The underlying mechanisms are to date controversial. A previously healthy 18-year-old female teenager affected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) developed fulminant cardiogenic shock requiring a prompt extracorporeal membrane oxygenation support. Cardiac involvement was predominant compared with the pulmonary one. Myocardial biopsies were performed; and in order to clarify the pathophysiology of the acute heart failure, optical and transmission electron microscopy study was realized. Two additional immunohistology techniques were developed in order to (i) detect a SARS-CoV-2 recombinant fusion nucleoprotein by using a specific antibody and (ii) study fractalkine expression induced by activated endothelium because this molecule is well known to be elevated in patients with severe cytokine release syndrome. SARS-CoV-2 genome was not detected in the myocardium. Even if the clinical presentation, laboratory markers, and cardiac imaging techniques strongly suggested fulminant myocarditis, histology and immunohistology were not fully consistent with this diagnosis according to the Dallas criteria. Although rare suspected coronavirus particles were found by transmission electron microscopy in the cardiac endothelium, neither significant immunoreactivity for the viral nucleocapsid protein nor image suggestive of endotheliitis was detected. Intense endothelial immunoreactivity pattern for fractalkine expression was observed. From a clinical point of view, the left ventricular systolic function gradually improved, and the patient survived after a long stay in the intensive care unit. Our observations suggest that a massive cytokine storm induced by SARS-CoV-2 infection was the main cause of the cardiogenic shock, making a direct viral injury pathway very unlikely.

A Belgian consensus strategy to identify familial hypercholesterolaemia in the coronary care unit and its subsequent cascade screening and treatment: BEL-FaHST (The BELgium Familial Hypercholesterolaemia STrategy).

BACKGROUND AND AIMS: Familial hypercholesterolaemia (FH) is an autosomal dominant lipoprotein disorder characterized by significant elevation of low-density lipoprotein cholesterol (LDL-C) and markedly increased risk of premature cardiovascular disease (CVD). Because of the very high coronary artery disease risk associated with this condition, the prevalence of FH among patients admitted for CVD outmatches many times the prevalence in the general population. Awareness of this disease is crucial for recognizing FH in the aftermath of a hospitalization of a patient with CVD, and also represents a unique opportunity to identify relatives of the index patient, who are unaware they have FH. This article aims to describe a feasible strategy to facilitate the detection and management of FH among patients hospitalized for CVD. METHODS: A multidisciplinary national panel of lipidologists, cardiologists, endocrinologists and cardio-geneticists developed a three-step diagnostic algorithm, each step including three key aspects of diagnosis, treatment and family care. RESULTS: A sequence of tasks was generated, starting with the process of suspecting FH amongst affected patients admitted for CVD, treating them to LDL-C target, finally culminating in extensive cascade-screening for FH in their family. Conceptually, the pathway is broken down into 3 phases to provide the treating physicians with a time-efficient chain of priorities. CONCLUSIONS: We emphasize the need for optimal collaboration between the various actors, starting with a "vigilant doctor" who actively develops the capability or framework to recognize potential FH patients, continuing with an "FH specialist", and finally involving the patient himself as "FH ambassador" to approach his/her family and facilitate cascade screening and subsequent treatment of relatives.

Detection and clinical usefulness of a biphasic response during exercise echocardiography early after myocardial infarction.

OBJECTIVE: The aim of this study was to determine the accuracy of exercise echocardiography (EE) for detecting infarct-related artery (IRA) stenosis and predicting functional recovery early after acute myocardial infarction (AMI). BACKGROUND: Dobutamine stress echocardiography is widely used for identifying jeopardized myocardium. The clinical usefulness of a biphasic response detected during EE has never been investigated. METHODS: A total of 114 consecutive patients with a first AMI and > or = 2 dyssynergic segments in the infarct-related territory underwent semi-supine continuous EE 6 +/- 2 days after AMI. Quantitative coronary angiography was performed in all patients after EE. A follow-up echocardiogram was obtained one month later. RESULTS: Ninety-seven patients had significant (> or = 50%) IRA stenosis, and 26 had multivessel disease. Residual ischemia was identified in 77 patients (biphasic response in 62 and worsening response in 15). The sensitivity and specificity of ischemia during EE for predicting IRA stenosis were 75% and 76%, respectively. The sensitivity of a biphasic response was higher than the sensitivity of a worsening response (61% vs. 14%, p < 0.0001). Wall motion abnormalities induced in other vascular territories were specific (97%) and moderately sensitive (62%) for the detection of multivessel disease. Functional recovery was observed in 75 patients. Two independent variables predicted contractile recovery: contractile reserve during EE (p < 0.0001) and elective angioplasty of the IRA (p = 0.002). A biphasic response, but not sustained improvement, predicted reversible dysfunction (73% vs. 9%, p < 0.0001). CONCLUSIONS: A biphasic response can be detected during exercise. Exercise echocardiography is an accurate tool for detecting IRA stenosis and predicting functional improvement early after AMI.

Prevalence of mechanical dyssynchrony in patients with heart failure and preserved left ventricular function (a report from the Belgian Multicenter Registry on dyssynchrony).

The present study evaluated the prevalence of mechanical inter- and intraventricular dyssynchrony in patients with heart failure and preserved left ventricular (LV) ejection fraction (LVEF). We studied 138 patients with heart failure (age 67+/-11 years; 76% men); 60 patients had preserved LVEF (>40%). Using conventional Doppler echocardiography, an interventricular mechanical delay>or=40 ms was defined as interventricular dyssynchrony. Using pulse-wave tissue Doppler imaging, the time from the beginning of the QRS complex to onset of systolic motion was measured in 4 basal LV segments. A dispersion of >or=60 ms was defined as intraventricular dyssynchrony. The prevalence of inter- and intraventricular dyssynchrony was lower in patients with preserved LVEF than in those with reduced LVEF (17% vs 41%, p<0.01 for interventricular dyssynchrony, 18% vs 36%, p<0.01 for intraventricular dyssynchrony). However, patients with preserved LVEF and a QRS width>or=120 ms had higher values for the parameters for inter- and intraventricular dyssynchrony than patients with a QRS width<120 ms (interventricular mechanical delay 33+/-20 vs 20+/-16 ms, p<0.05; tissue Doppler imaging dispersion 42+/-26 vs 33+/-22 ms, p<0.05). In patients with a QRS width>or=120 ms, the prevalence of inter- and intraventricular dyssynchrony was comparable for patients with preserved and reduced LVEF (42% vs 55%, p=NS for interventricular dyssynchrony and 45% vs 46%, p=NS for intraventricular dyssynchrony). In conclusion, the prevalence of inter- and intraventricular dyssynchrony was low (17% and 18%, respectively) in patients with heart failure and preserved LVEF. However, in the presence of a QRS width of >or=120 ms, this prevalence increased to almost 50%, comparable to that for patients with heart failure and reduced LVEF and a QRS width of >or=120 ms.

Long-term effect of molsidomine, a direct nitric oxide donor, as an add-on treatment, on endothelial dysfunction in patients with stable angina pectoris undergoing percutaneous coronary intervention: results of the MEDCOR trial.

OBJECTIVE: The MEDCOR trial is a double-blind, randomized study aiming at demonstrating the superiority of molsidomine (direct NO donor) over placebo, used as add-on treatments, on improving endothelial function (EF) after 12 months, in stable angina patients undergoing percutaneous coronary intervention. METHODS: EF was assessed by peripheral vasodilator response (i.e. Endoscore) using arterial tonometry and by several biomarkers, in terms of changes versus baseline after a one-year treatment. RESULTS: The change in Endoscore was +75 ± 130% in placebo group and +39 ± 145% in molsidomine group (p = 0.143). There was a decrease in sICAM-1 with molsidomine (-6%) and an increase with placebo (+6%). The MPO activity/antigen ratio slightly increased with placebo (+9%) and strongly decreased with molsidomine (-42%) (p = 0.020). CONCLUSION: The MEDCOR trial was not able to demonstrate significant differences between molsidomine and placebo for all parameters, except the MPO activity/antigen ratio which significantly decreased with molsidomine (p = 0.020 versus placebo).

Short-term effect of atorvastatin on ischaemic threshold in hypercholesterolaemic patients with stable ischaemic heart disease.

OBJECTIVE: Hypercholesterolaemia is associated with a loss of endothelium-dependent vasodilation, which may facilitate the occurrence of myocardial ischaemia in patients with coronary artery disease (CAD). The improvement of endothelial dilator function after 4 to 6 weeks of oral lipid-lowering therapy has been documented. Whether this early restoration of endothelial function by statins translates into anti-ischaemic effects is unknown. This study was designed to determine the effect of 4 weeks' treatment with 80 mg atorvastatin daily on exercise-induced ischaemia in patients with stable ischaemic heart disease (IHD) receiving standard anti-anginal drug therapy. METHODS AND RESULTS: A total of 41 patients with documented CAD, exercise-induced ischaemia and LDL-cholesterol > 130 mg/dl underwent exercise ECG, angina score and lipid level assessment at baseline, after 4 weeks of placebo treatment, and after 4 weeks of therapy with atorvastatin 80 mg. Primary endpoint was the change in time to 1 mm ST-segment depression (= ischaemic threshold) between placebo and treatment period. Atorvastatin treatment resulted in a 55% reduction of low-density lipoprotein (LDL) cholesterol (from mean of 162 (SD 32) to 72 (20) mg/dl). For a comparable rate-pressure product, the average time to 1 mm ST-segment depression was 295 (112) s at baseline, 314 (149) s after placebo and 301 (131) s after atorvastatin, indicating that the ischaemic threshold was not significantly modulated after 4 weeks of atorvastatin treatment. There was also no significant change in global angina score or in time to maximal ST-segment depression. CONCLUSIONS: High-dose atorvastatin treatment for 4 weeks drastically reduced LDL-cholesterol. However, the present study did not demonstrate a significant effect on the ischaemic threshold in patients with stable IHD already under treatment with anti-ischaemic agents.

Double-blind parallel placebo-controlled study to evaluate the effect of molsidomine on the endothelial dysfunction in patients with stable angina pectoris undergoing percutaneous coronary intervention: the MEDCOR Trial.

The effects of molsidomine (a direct nitric oxide donor) on the endothelial dysfunction have never been evaluated using reactive hyperemia peripheral arterial tonometry (RH-PAT). The objective of the MEDCOR double-blind trial will be to demonstrate the superiority of molsidomine (Coruno® 16 mg, once daily) over placebo, on improving the endothelial function (Endoscore by RH-PAT) after 12 months of treatment in stable angina patients undergoing elective percutaneous coronary intervention (PCI). Study design will take care of the real-life situation, in which patients are being offered PCI and stent placement (drug-eluting or bare metal), but also gold standard medical therapy (beta-blockers, statins, angiotensin-converting enzyme inhibitors (ACEIs), and/or calcium antagonists). Demonstrating clinical and statistical superiority of the study drug over placebo will be a real challenge. Therefore, a sequential approach has been designed with a pilot phase aiming at recruiting 50 patients. Upon evaluation of the results by an independent data steering committee, a larger sample size phase will eventually be considered.