ABSTRACT
It has been well established that arterial hypertension is considered as a predominant risk factor for the development of cardiovascular diseases. Despite the link between arterial hypertension and cardiovascular diseases, arterial hypertension may directly affect cardiac function, leading to heart failure, mostly with preserved ejection fraction (HFpEF). There are echocardiographic findings indicating hypertensive heart disease (HHD), defined as altered cardiac morphology (left ventricular concentric hypertrophy, left atrium dilatation) and function (systolic or diastolic dysfunction) in patients with persistent arterial hypertension irrespective of the cardiac pathologies to which it contributes, such as coronary artery disease and kidney function impairment. In addition to the classical echocardiographic parameters, novel indices, like speckle tracking of the left ventricle and left atrium, 3D volume evaluation, and myocardial work in echocardiography, may provide more accurate and reproducible diagnostic and prognostic data in patients with arterial hypertension. However, their use is still underappreciated. Early detection of and prompt therapy for HHD will greatly improve the prognosis. Hence, in the present review, we shed light on the role of echocardiography in the contemporary diagnostic and prognostic approaches to HHD.
ABSTRACT
Pheochromocytoma-induced Takotsubo cardiomyopathy is a rare but life-threatening condition, caused by excessive plasma catecholamine levels, resulting in acute myocardial dysfunction. Clinical presentation includes a rapid development of heart failure due to regional wall motion abnormalities (most commonly affecting all mid to apical left ventricle (LV) wall segments) causing the "octopus-trap-like" LV shape. A 45-year-old female patient presented with acute cardiogenic shock of non-ischemic etiology. Her past medical history included a similar episode, which was followed by full recovery, but at this admission she required hemodynamic support with venoarterial extracorporeal membrane oxygenation. The systolic function was restored, and further investigation revealed high 24-h urine metanephrine levels and a mass of the left adrenal gland, leading to the diagnosis of pheochromocytoma. After treatment with firstly alpha-blockers and then beta-blockers, the pheochromocytoma was surgically removed.
ABSTRACT
The right heart catheterisation constitutes the gold standard for pulmonary hypertension (PH) diagnosis. However, echocardiography remains a reliable, non-invasive, inexpensive, convenient, and easily reproducible modality not only for the preliminary screening of PH but also for PH prognosis. The aim of this review is to describe a cluster of echocardiographic parameters for the detection and prognosis of PH and analyse the challenges of echocardiography implementation in patients with suspected or established PH. The most important echocardiographic index is the calculation of pulmonary arterial systolic pressure (PASP) through the tricuspid regurgitation (TR). It has shown high correlation with invasive measurement of pulmonary pressure, but several drawbacks have questioned its accuracy. Besides this, the right ventricular outflow track acceleration time (RVOT-AT) has been proposed for PH diagnosis. A plethora of echocardiographic indices: right atrial area, pericardial effusion, the tricuspid annular plane systolic excursion (TAPSE), the TAPSE/PASP ratio, tricuspid annular systolic velocity (s'), can reflect the severity and prognosis of PH. Recent advances in echocardiography with 3-dimensional right ventricular (RV) ejection fraction, RV free wall strain and right atrial strain may further assist the prognosis of PH.
ABSTRACT
The role of inflammation in the pathophysiology of acute myocardial infarction (AMI) is well established. In recognizing inflammation's pivotal role in AMI, this manuscript systematically traces the historical studies spanning from early attempts to the present landscape. Several anti-inflammatory trials targeting inflammation in post-AMI have been performed, and this review includes the key trials, as well as examines their designs, patient demographics, and primary outcomes. Efficacies and challenges are analyzed, thereby shedding light on the translational implications of trial outcomes. This article also discusses emerging trends, ongoing research, and potential future directions in the field. Practical applications and implications for clinical practice are considered by providing a holistic view of the evolving landscape of anti-inflammatory interventions in the context of AMI.
ABSTRACT
BACKGROUND: Several studies showed serum markers elevation as a result to coronary angiography. We investigated the effect of diagnostic coronary angiography (DCA) on the development of systemic inflammatory response syndrome (SIRS) and on whole blood cytokine production capacity after ex-vivo LPS stimulation. METHODS: In this observational study, clinical characteristics and serum cytokines of the patients were recorded at baseline and at 2, 6, 12, and 24h after DCA. Peripheral blood was collected at baseline and at 2, and 24h for complete blood count, coagulation profile and ex-vivo (100 microl) stimulation with LPS (500 pg) for subsequent cytokine measurement. Values are expressed as median+/-IQR and were compared using Wilcoxon's signed rank test with Bonferroni adjustment. RESULTS: We included 23 male patients (mean age 52.0+/-18.0 years) undergoing DCA. None of the patients developed clinical or laboratory signs of SIRS. Serum IL-6 significantly increased at 12h. There was a significant decrease in TNF-alpha production after ex-vivo LPS stimulation of whole blood at 2 and 24h compared to baseline (median+/-IQR; 716.0+/-319.0; 576.0+/-715.0 vs. 1154+/-844.0 pg/ml; respectively) suggesting that DCA may cause transient endotoxin tolerance. CONCLUSIONS: DCA is related to increased serum IL-6 levels but does not cause clinical SIRS. Development of SIRS after DCA is indicative of other in origin complication. DCA is associated with immune cells hyporesponsiveness, possibly through monocyte depression, expressed as decreased TNF-alpha production after whole blood stimulation with LPS ex vivo.