Kan Liu

Obesity hypertension: the regulatory role of leptin.

Leptin is a 16-kDa-peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake and elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. While the relevance of endogenous leptin needs further clarification, it appears to function as a pressure and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular, and cardiac damage.

Cardiac Troponins: Bench to Bedside Interpretation in Cardiac Disease

Abstract:Cardiac troponins are the preferred biomarkers for the determination of acute myocardial necrosis. The high sensitivity of the available assays has significantly increased the detection of microscopic amounts of myocardial damage. Although compelling evidence indicates that elevated cardiac troponins are markers of poor prognosis and increased mortality, irrespective of the clinical scenario, small elevations can be seen in protean conditions and may confound the diagnosis of acute coronary syndromes. Emerging evidence suggests multiple different cellular mechanisms leading to cardiac troponin release, which challenge long held paradigms such as equivalency between troponin release into the circulation and irreversible cell death. Hence, knowledge of the physiology and pathophysiology of these cardiac biomarkers is essential for their accurate interpretation and consequent correct clinical diagnosis. Herein, the current relevant information about cardiac troponins is discussed, with special emphasis on pathophysiology and clinical correlates.

The Cardiorenal Syndrome in Heart Failure: An Evolving Paradigm

Heart failure constitutes a significant source of morbidity and mortality in the United States, and its incidence and prevalence continue to grow, increasing its burden on the healthcare system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phenomenon characterized by a pathophysiologic disequilibrium between the heart and the kidney, in which malfunction of 1 organ consequently promotes the impairment of the other. Multiple neurohumoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is recommended to achieve optimal results.

The kidney in heart failure: friend or foe?

Abstract:Heart failure constitutes a significant source of morbidity and mortality in the United States and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associated with adverse clinical outcomes. This complex interaction is characterized by a pathophysiological disequilibrium between the heart and the kidney, in which cardiac malfunction promotes renal impairment, which in turn feeds back for further deterioration of cardiovascular function. Multiple neurohumoral and hemodynamic mechanisms are involved in this cardiorenal dyshomeostasis, including the deficiency of and/or resistance to compensatory natriuretic peptides, leading to sodium retention, volume overload and organ remodeling. Management of patients with cardiorenal dysfunction can be challenging and should be individualized. Emerging therapies must address the impairment of both organs to secure better clinical outcomes. To this end, a multidisciplinary approach is warranted to achieve optimal results.

Obesity Hypertension: Pathophysiological Role of Leptin in Neuroendocrine Dysregulation

Abstract:Leptin is a 16-kDa peptide hormone that is primarily synthesized and secreted by adipose tissue. One of the major actions of this hormone is the control of energy balance by binding to receptors in the hypothalamus, leading to reduction in food intake, elevation in temperature and energy expenditure. In addition, increasing evidence suggests that leptin, through both direct and indirect mechanisms, may play an important role in cardiovascular and renal regulation. Although the relevance of endogenous leptin needs further clarification, it appears to function as a pressure- and volume-regulating factor under conditions of health. However, in abnormal situations characterized by chronic hyperleptinemia such as obesity, it may function pathophysiologically for the development of hypertension and possibly also for direct renal, vascular and cardiac damage.

A 54-year-old man with new-onset ventricular fibrillation

Clinical introduction A 54-year-old man without significant medical history presented with sudden-onset chest discomfort and multiple episodes of ventricular fibrillation requiring external defibrillation and cardiopulmonary resuscitation. Coronary angiography ruled out significant artery stenosis. Both ventriculography and echocardiography revealed decreased left ventricular ejection fraction (25%). On examination, he was haemodynamically stable. The lungs were clear to auscultation and there was no jugular venous dilation. The cardiac examination revealed a regular rate and rhythm without murmur. Cardiac magnetic resonance (CMR) and 18F-2-fluoro-2-deoxyglucose positron emission tomography (FDG-PET) images were shown (figure 1). Figure 1 Cardiac magnetic resonance with a T1-weighted inversion recovery image (A) and 18F-2-fluoro-2-deoxyglucose positron emission tomography (B) in a 54-year-old man with new-onset ventricular fibrillation. Question Which of the following would be the next best step? Implantable loop recorder Electrophysiological testing for radiofrequency catheter ablation Endomyocardial biopsy Genetic testing

Pulmonary Arterial Hypertension versus Pulmonary Venous Hypertension: How Much Information Can Contrast Doppler Echocardiography Provide?

In the Dec 10, 2012 issue of Echocardiography, Taleb et al. performed a very interesting metaanalysis to estimate the diagnostic accuracy of Doppler echocardiography (DE) to assess pulmonary arterial systolic pressure (PASP) and to diagnose pulmonary hypertension (PH). They concluded that the sensitivity, specificity, and accuracy of DE for the diagnosis of PH were 88%, 56%, and 63%, respectively. However, we hope to point out that these results come from DE studies done between 1984 and 2009, most of which had been performed before echocardiographic contrast agents became available. The PASP relies largely on accurate assessment of

El síndrome cardiorenal en insuficiencia cardíaca: Un paradigma en evolución

Heart failure constitutes a significant source of morbidity and mortality in the United Sta-tes and its incidence and prevalence continue to grow, increasing its burden on the health care system. Renal dysfunction in patients with heart failure is common and has been associatedwith adverse clinical outcomes. This interaction, termed the cardiorenal syndrome, is a complex phe-nomenon characterized by a pathophysiological dise-quilibrium between the heart and the kidney, in which malfunction of one organ subsequently promotes the impairment of the other.Multiple neuro-humoral mechanisms are involved in this cardiorenal interaction, including the deficiency of and/or resistance to compensatory natriuretic pepti-des, leading to sodium retention, volume overload and organ remodeling. Management of patients with the cardiorenal syndrome can be challenging and should be individualized. Emerging therapies must address the function of both organs in order to secure better clinical outcomes. To this end, a multidisciplinary ap-proach is recommended to achieve optimal results.

Mechanical interventricular dependency supports hemodynamics in tako-tsubo cardiomyopathy

Background Although morphological abnormalities of the heart appear to be remarkable, most patients with tako-tsubo cardiomyopathy (TTC) remain clinically stable. We investigate real time changes in the left ventricular (LV) and right ventricular (RV) mechanics and function to explore the mechanism to preserve hemodynamics. Methods With deformation and Doppler echocardiography, we evaluated myocardial mechanics and ventricular function/hemodynamics simultaneously in 103 consecutive TTC patients admitted from 01/01/2008 through 12/31/2015. The coronary angiography and left ventriculography were performed to rule out culprit coronary artery stenosis (CAS). We included 66 patients in a control group with matched age, sex, and risk factors for coronary artery disease (CAD), and 41 patients in a group of myocardial infarction induced cardiogenic shock, who required circulatory supporting devices to maintain hemodynamic stability. Results Although systolic myocardial strain in most of the LV segments was significantly impaired, 4 basal LV segments remained functionally active during acute stage of TTC. The impairment in the myocardial strain of the RV apex could extend to the middle segments, but basal RV systolic strain was also preserved. Despites comparable apical to basal strain gradients, LV and RV displayed discrepant functional/hemodynamic status. In contrast to LV, RV functional/hemodynamic parameters appeared to be hyper-dynamic. This unique RV strain pattern remained unchanged in patients with atypical (mid-LV cavity) TTC. In 41 patients with myocardial infarction induced cardiogenic shock, RV exhibited comparable mechanic and functional features with those in TTC patients. Conclusions The identified LV and RV mechanic changes appear to support interventricular hemodynamic dependence during TTC, which may represent a universal rescue mechanism in a jeopardized or injured heart.

Myocardial contractile patterns predict future cardiac events in sarcoidosis

The poor prognosis of cardiac sarcoidosis (CS) underscores the need for risk stratification. We evaluated 84 consecutive sarcoidosis patients who were referred for echocardiographic studies for cardiac symptoms or abnormal electrocardiograms. In 54 patients without previous diagnosis of CS or other known structural heart disease, 13 reached endpoints during (median) 24 months follow up. Significantly impaired peak systolic longitudinal strain in their original echocardiograms were identified in 13 of 17 left ventricular segments, clustering in the free wall, interventricular septum and apex. The regional (including 13 clustered segments) peak systolic longitudinal strain (RPSLS) were significantly impaired in patients with endpoints, compared with those without [(−11.4 ± 4.45) vs. (−18.7 ± 3.76) %, P < 0.00001]. Cox multivariate regression analysis revealed that RPSLS was independently associated with endpoints (HR 1.24; 95% CI 1.08–1.42, P = 0.002). Receiver operating characteristic curve suggested a cut-off RPSLS value of −15.0% (84.6% sensitivity and 86.8% specificity) to predict the occurrence of endpoints. Impaired RPSLS correlates with risk of adverse cardiac events in patients with extra-cardiac sarcoidosis.