Mankad, Sunil

Sepsis continues to be a leading cause of mortality and morbidity in the intensive care unit. Cardiovascular dysfunction in sepsis is associated with worse short- and long-term outcomes. Sepsis-related myocardial dysfunction is noted in 20%–65% of these patients and manifests as isolated or combined left or right ventricular systolic or diastolic dysfunction Echocardiography is the most commonly used modality for the diagnosis of sepsis-related myocardial dysfunction. With the increasing use of ultrasonography in the intensive care unit, there is a renewed interest in sepsis-related myocardial dysfunction. This review summarises the current scope of literature focused on sepsis-related myocardial dysfunction and highlights the use of basic and advanced echocardiographic techniques for the diagnosis of sepsis-related myocardial dysfunction and the management of sepsis and septic shock.

Numerous strategies have been evaluated to prevent early CSA-AKI. Although correction of hemodynamic problems is paramount, there are no clinical studies that compare different hemodynamic management or monitoring strategies with regard to their effect on kidney function. Pharmacologic strategies including diuretics, different classes of vasodilators and drugs with anti-inflammatory effects such as N-acetyl-cysteine, do not appear to be effective. Most of the studies are underpowered and use physiological rather than clinical endpoints. Further trials are warranted with fenoldopam and nesiritide (rhBNP). Observational and underpowered randomized studies show beneficial renal effects of off-pump technique and avoidance of aortic manipulation. There is very limited evidence for preoperative fluid loading and preemptive RRT. Potentially nephrotoxic agents should be used with caution in patients at risk of CSA-AKI. Tranexamic acid or aminocaproic acid should be preferred over aprotinin. No pharmacologic intervention has been adequately tested in the prevention of late CSA-AKI. A single-center study, including a predominance of patients after cardiac surgery, showed a decrease of kidney injury with tight glycemic control.

Despite its high prevalence, little is known about mechanisms of mitral regurgitation in degenerative mitral valve disease apart from the leaflet prolapse itself. Mitral valve is a complex structure, including mitral annulus, mitral leaflets, papillary muscles, chords, and left ventricular walls. All these structures are involved in physiological and pathological functioning of this valvuloventricular complex but up to now were difficult to analyze because of inherent limitations of 2-dimensional imaging. The advent of 3-dimensional echocardiography, computed tomography, and cardiac magnetic resonance imaging overcoming these limitations provides new insights into mechanistic analysis of degenerative mitral regurgitation. This review will detail the contribution of quantitative and qualitative dynamic analysis of mitral annulus and mitral leaflets by new imaging methods in the understanding of degenerative mitral regurgitation pathophysiology.

BackgroundPatients with heart failure (HF) have increased risk for thromboembolic events. Real‐world incidences of efficacy and safety outcomes of direct oral anticoagulants (DOACs) in patients with left ventricular systolic dysfunction (LVSD) are of growing clinical interest.HypothesisReal‐world efficacy and safety outcomes of DOACs in patients with LVSD will be similar to those of LVSD or HF subgroups in the RE‐LY, ROCKET‐AF, and ARISTOTLE trials.MethodsWe performed a retrospective review of adult patients with LVSD (left ventricular ejection fraction ≤40%) on DOAC therapy between 2010 and 2016. Incidences of safety and efficacy outcomes of anticoagulation with DOACs were extracted from primary and secondary hospital discharge diagnoses.ResultsDOACs were prescribed to 287 patients with LVSD over a mean follow‐up of 313.3 ± 52.3 days. Many patients had moderate and severe chronic kidney disease (28.9% and 10.1%, respectively) and indications for anticoagulation therapy other than atrial fibrillation (19.9%). For efficacy outcomes, the calculated incidence rates of ischemic stroke and systemic embolism were 1.2 (95% confidence interval [CI]: 0.25‐3.56) and 0.81 (95% CI: 0.10‐2.94) events per 100 person‐years, respectively. For the safety outcomes, incidence rates of GI bleeding and intracranial hemorrhage were 2.4 (95% CI: 0.8‐5.3) and 0.41 (95% CI: 0.1‐2.2) events per 100 patient‐years, respectively.ConclusionsOur findings are largely compatible with the results of LVSD or HF subgroups in RE‐LY, ROCKET‐AF, and ARISTOTLE trials and add to increasing confidence that DOACs can be safely used for stroke and systemic embolism prevention in patients with LVSD.

BackgroundAcute myocardial infarctions (AMI) continue to be common in the United States. Mechanical complications of AMI can lead to cardiogenic shock (CS) and death. The aim of this study was to review the cases of papillary muscle ruptures in the setting of myocardial infarctions at a tertiary care center, with a focus on the clinical presentation and echocardiographic diagnosis.MethodsThis was a retrospective study from January 1, 2000 through December 31, 2014. In all, 22 patients with AMI and papillary muscle rupture (AMI‐PMR) who had surgical intervention were identified.ResultsThe average age was 70 (±11) with 16 (73%) males. Six patients presented with ST‐elevation myocardial infarctions (STEMI) and all underwent emergent revascularization with primary percutaneous coronary intervention (PCI) prior to the diagnosis of AMI‐PMR. The other 16 patients presented with a non‐STEMI. In total, 17 (77%) of the 22 patients were diagnosed with an AMI‐PMR within 7 days from their onset of symptoms. In all, 12 patients (55%) had anterolateral papillary muscle ruptures (ALPMR), and the other 10 had posteromedial papillary muscle ruptures (PMPMR). Ruptures were complete in 10 patients (45%). Patients presented with pulmonary edema early (<7 days) more commonly than late (>14 days). Transthoracic echocardiography was able to demonstrate severe mitral regurgitation in 86% and a definitive or suggestive diagnosis in 93%. All 22 patients survived to operative management, and the overall in‐hospital mortality rate was 9%.ConclusionIn conclusion, ischemic papillary muscle ruptures continue to occur, but with prompt diagnosis by echocardiography and rapid surgical management, the mortality rate continues to decline.

Hypereosinophilic syndrome (HES) is a heterogeneous group of conditions that is defined at its core by hypereosinophilia (HE) (blood eosinophil count of >1.5×10 9 /L) and organ damage directly attributable to the HE. Cardiac dysfunction occurs frequently in all forms of HES and is a major cause of morbidity and mortality. Once a significantly elevated eosinophil count is identified, it must be confirmed on repeat testing and the aetiology for the HE must be rigorously sought out with a focus on identifying whether organ dysfunction is occurring. Echocardiography is routinely performed to assess for cardiac involvement, looking for evidence of left ventricular and/or right ventricular apical obliteration or thrombi or a restrictive cardiomyopathy. Cardiac magnetic resonance imaging and CT are often useful adjuncts to establish the diagnosis but endomyocardial biopsy remains the gold standard. To decrease the degree of eosinophilia, treatment can include corticosteroids and/or imatinib based on the aetiology. Anticoagulation, standard heart failure therapy for a restrictive cardiomyopathy and finally cardiac transplantation may be indicated in the treatment algorithm.