Growth Differentiation Factor 15: A Prognostic Marker in Patients with Acute Chest Pain without Acute Myocardial Infarction.

BACKGROUND: Acute chest pain is associated with an increased risk of death and cardiovascular events even when acute myocardial infarction (AMI) has been excluded. Growth differentiation factor-15 (GDF-15) is a strong prognostic marker in patients with acute chest pain and AMI, but the prognostic value in patients without AMI is uncertain. This study sought to investigate the ability of GDF-15 to predict long-term prognosis in patients presenting with acute chest pain without AMI. METHODS: In total, 1320 patients admitted with acute chest pain without AMI were followed for a median of 1523 days (range: 4 to 2208 days). The primary end point was all-cause mortality. Secondary end points included cardiovascular (CV) death, future AMI, heart failure hospitalization, and new-onset atrial fibrillation (AF). RESULTS: Higher concentrations of GDF-15 were associated with increased risk of death from all causes (median concentration in non-survivors vs survivors: 2124 pg/mL vs 852 pg/mL, P < 0.001), and all secondary end points. By multivariable Cox regression, GDF-15 concentration ≥4th quartile (compared to <4th quartile) remained an independent predictor of all-cause death (adjusted hazard ratio (HR): 2.75; 95% CI, 1.69-4.45, P < 0.001), CV death (adjusted HR: 3.74; 95% CI, 1.31-10.63, P = 0.013), and heart failure hospitalization (adjusted HR: 2.60; 95% CI, 1.11-6.06, P = 0.027). Adding GDF-15 to a model consisting of established risk factors and high-sensitivity cardiac troponin T (hs-cTnT) led to a significant increase in C-statistics for prediction of all-cause mortality. CONCLUSIONS: Higher concentrations of GDF-15 were associated with increased risk of mortality from all causes and risk of future CV events.

A case report of giant cell myocarditis complicated by severe heart failure: the value of early endomyocardial biopsy and mechanical circulatory support.

Background: Giant cell myocarditis (GCM) is a rare, probably underdiagnosed and potentially fatal disease in young and middle-aged patients. Disease progression is often rapid, and life-threatening arrhythmias and cardiogenic shock due to progressive left ventricular failure are among the most feared complications. Although cardiac biomarkers and multimodality imaging are used as initial diagnostic tests in most patients, endomyocardial biopsy (EMB) is often required for a definitive diagnosis. However, there are still gaps in our knowledge in terms of the etiology, early diagnosis, management and prognosis of GCM. Case Description: We present the case of a male patient in his early 50s admitted to Haukeland University Hospital with fulminant GCM. He had no significant medical history in the past apart from hypertension, and presented to hospital in cardiogenic shock after a few weeks of progressive shortness of breath. Rapid initiation of methylprednisolone had an immediate effect on reducing myocardial inflammation, and sustained treatment with a combination of immunosuppressive agents along with optimal heart failure medications led to complete recovery of the heart function and clinical remission over several years. The case study highlights the urgency of an early EMB, access to mechanical circulatory support (MCS) and the efficacy of immunosuppressive treatment and optimal medical management for heart failure. Finally, our review of the literature also provides an updated guidance on the contemporary management of GCM patients. Conclusions: Accurate and early diagnosis with EMB in patients with GCM are crucial for better outcomes. Rapid initiation of methylprednisolone reduces myocardial inflammation and the risk of death. Sustained treatment with a combination of immunosuppressive agents together with optimal heart failure medications are essential for myocardial recovery and long-term stabilization. The use of MCS is the cornerstone in the management of GCM with a clear survival benefit.

An Unexpected Cause of Severe Hypertension and Bradycardia: The Role of Hemodynamic Assessment by Echocardiography.

Severe hypertension has numerous etiologies. When accompanied by bradycardia, the spectrum of differential diagnoses is greatly narrowed and is commonly seen in patients with increased intracranial pressure. However, other etiologies such as bradycardia-induced hypertension are rarely mentioned. Here we report the case of a 73-year-old woman presenting with symptoms of heart failure, severe hypertension, and bradycardia with a 2:1 atrioventricular block. Echocardiography demonstrated increased left ventricular filling secondary to bradycardia and prolonged diastole, leading to greater ventricular stretch, increased contractile force and greater stroke volume (Frank-Starling mechanism), which subsequently caused elevated systolic blood pressure (BP), low diastolic BP and a wide pulse pressure. Treating the bradycardia by pacing led to an immediate and substantial BP reduction, although complete BP normalization had a slower time course and was probably due to the concomitant effect of the antihypertensive treatment initiation. This pathophysiological mechanism has received little attention in the literature. Further, stimulation of sympathetic afferents located in the heart by distension of the cardiac walls as well as the role of vagally innervated cardiopulmonary receptors due to the increased pressure in the heart and the pulmonary artery should also be kept in mind as alternative hypotheses.