Assessment of Left Atrial Deformation and Function by 2-Dimensional Speckle Tracking Echocardiography in Healthy Dogs and Dogs With Myxomatous Mitral Valve Disease

open7noBackground: The assessment of left atrial (LA) function by 2-dimensional speckle tracking echocardiography (STE) holds important clinical implications in human medicine. Few similar data are available in dogs. Objectives: To assess LA function by STE in dogs with and without myxomatous mitral valve disease (MMVD), analyzing LA areas, systolic function, and strain. Animals: One hundred and fifty dogs were divided according to the American College of Veterinary Internal Medicine classification of heart failure: 23 dogs in class A, 52 in class B1, 36 in class B2, and 39 in class C + D. Methods: Prospective observational study. Conventional morphologic and Doppler variables, LA areas, and STE-based LA strain analysis were performed in all dogs and results were compared among groups. Correlation analysis was carried out between LA STE variables and other echocardiographic variables. Results: Variability study showed good reproducibility for all the tested variables (coefficient of variation <16%). Left atrial areas, fractional area change, peak atrial longitudinal strain (PALS), peak atrial contraction strain, and contraction strain index (CSI) differed significantly between groups B2 and C + D and all the other groups (overall P < .001), whereas only PALS differed between groups B1 and A (P = .01). Left atrial areas increased with progression of the disease, whereas LA functional parameters decreased. Only CSI increased nonsignificantly from group A to group B1 and then progressively decreased. Thirty-one significant correlations (P < .001, r > .3) were found between conventional left heart echocardiographic variables and LA areas and strain variables. Conclusions and Clinical Importance: Left atrial STE analysis provides useful information on atrial function in the dog, highlighting a progressive decline in atrial function with worsening of MMVD.openBaron Toaldo, M; Romito, G.; Guglielmini, C.; Diana, A.; Pelle, N.G.; Contiero, B.; Cipone, M.Baron Toaldo, M; Romito, G.; Guglielmini, C.; Diana, A.; Pelle, N.G.; Contiero, B.; Cipone, M

Determinants of Pulmonary Hypertension in Left Ventricular Dysfunction

AbstractObjectives. This study sought to analyze the determinants of pulmonary hypertension in patients with left ventricular dysfunction.Background. Pulmonary hypertension in patients with left ventricular dysfunction is a predictor of poor outcome. The independent role of cardiac functional abnormalities in the genesis of pulmonary hypertension is unclear.Methods. In 102 consecutive patients with primary left ventricular dysfunction (ejection fraction <50%), systolic pulmonary artery pressure was prospectively measured by Doppler echocardiography (using tricuspid regurgitant velocity), and left ventricular systolic and diastolic function, functional mitral regurgitation, cardiac output and left atrial volume were quantified.Results. Systolic pulmonary artery pressure was elevated in patients with left ventricular dysfunction (51 ± 14 mm Hg [mean ± SD]), but the range was wide (23 to 87 mm Hg). Of the numerous variables correlating significantly with systolic pulmonary artery pressure, the strongest were mitral deceleration time (r = −0.61, p = 0.0001; odds ratio of pulmonary pressure ≥50 mm Hg [95% confidence interval] if <150 ms, 48.8 [14.8 to 161]) and mitral effective regurgitant orifice (r = 0.50, p = 0.0001; odds ratio [95% confidence interval] if ≥20 mm2, 5.9 [2.3 to 15.5]). In multivariate analysis, these two variables were the strongest predictors of systolic pulmonary artery pressure in association with age (p = 0.005). Ejection fraction or end-systolic volume was not an independent predictor of pulmonary artery pressure.Conclusions. Pulmonary hypertension is frequent and highly variable in patients with left ventricular dysfunction. It is not independently related to the degree of left ventricular systolic dysfunction but is strongly associated with diastolic dysfunction (shorter mitral deceleration time) and the degree of functional mitral regurgitation (larger effective regurgitant orifice). These results emphasize the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.(J Am Coll Cardiol 1997;29:153–9)

Assessing and grading congestion in acute heart failure: a scientific statement from the acute heart failure committee of the heart failure association of the European society of cardiology and endorsed by the European society of intensive care medicine

Patients with acute heart failure (AHF) require urgent in-hospital treatment for relief of symptoms. The main reason for hospitalization is congestion, rather than low cardiac output. Although congestion is associated with a poor prognosis, many patients are discharged with persistent signs and symptoms of congestion and/or a high left ventricular filling pressure. Available data suggest that a pre-discharge clinical assessment of congestion is often not performed, and even when it is performed, it is not done systematically because no method to assess congestion prior to discharge has been validated. Grading congestion would be helpful for initiating and following response to therapy. We have reviewed a variety of strategies to assess congestion which should be considered in the care of patients admitted with HF. We propose a combination of available measurements of congestion. Key elements in the measurement of congestion include bedside assessment, laboratory analysis, and dynamic manoeuvres. These strategies expand by suggesting a routine assessment of congestion and a pre-discharge scoring system. A point system is used to quantify the degree of congestion. This score offers a new instrument to direct both current and investigational therapies designed to optimize volume status during and after hospitalization. In conclusion, this document reviews the available methods of evaluating congestion, provides suggestions on how to properly perform these measurements, and proposes a method to quantify the amount of congestion presen

Collateral cardiovascular damage in inflammatory joint diseases:Focus on cardiac dysfunction

This thesis aims to improve knowledge about the role of systemic inflammation in the development of cardiovascular disease and particularly cardiac dysfunction. Furthermore, to elucidate the added value of cardiac screening in this population. In Part I of this thesis including chapters 2-5, we focus on the role of inflammation in the development of CVD in IJD patients. Chapter 2 describes the prevalence, pathophysiology, and guidelines for CVD in IJD, i.e. RA and gout. In chapter 3 we reviewed the current literature on the effect of anti-inflammatory treatment, i.e. anti-TNF, on the cardiac function and the prevalence and incidence of CHF in RA. We performed echocardiography to assess the effect of anti-TNF on the cardiac function in RA patients with active disease in chapter 4. Part I finishes with chapter 5 describing a case report of a SLE patient with SLE induced heart failure with preserved ejection fraction (HFpEF) where the heart failure was treated with anti-inflammatory therapy. In part II, we focus on the role of systemic inflammation and cardiac diseases in AS patients. In this light, in chapter 6, we performed a large cross-sectional study in AS patients and osteoarthritis (OA) controls, the CARDAS study, to assess the prevalence of cardiac valve disease, conduction disturbances and cardiac dysfunction in AS. In our aim to identify a subgroup of AS patients at risk for aortic valve disease, in chapter 7, we performed a sub study of the CARDAS study to assess the association between HLAB27 genotype and aortic root dilatation and aortic valve regurgitation. Finally, part III reports on clinical trials focusing on relation between systemic inflammation and cardiovascular disease beyond the heart. In chapter 8, we conducted a cross-sectional controlled study in AS patients and healthy controls to assess the difference in retinal vasculature and to assess the value of retinal screening for cardiovascular disease. Furthermore, we assessed the effect of anti-inflammatory therapy on insulin resistance and body composition in RA patients in chapter 9

The effects of nicotine and cigarette smoking on cardiac electrophysiology.

Cigarette smoking is a leading cause of preventable disease and premature death worldwide. The adverse effects of cigarette smoking, including proarrhythmia, are related to the mixture of chemicals, including nicotine (which sustains tobacco addiction). However, it remains unclear which individual tobacco smoke constituents and biological pathways mediate this increased risk. The purpose of this research was to explore the chronic effects of cigarette smoking, as well as compare the acute effects of nicotine and cigarette smoking, and the possible role of β-adrenoreceptors, on human cardiac electrophysiology. Chapter 1 is a comprehensive literature review of (a) the ex vivo and in vivo effects of nicotine and non-nicotine constituents of cigarette smoking on cardiac ion channels, (b) the direct and indirect effects of the autonomic nervous system on cardiac electrophysiology, and (c) studies of acute and chronic effects of cigarette smoking in humans. Chapter 2 consists of two studies in which we used cotinine levels to investigate the differences in baseline cardiac electrocardiogram between chronic smokers and non-smokers, and to define smoking status and its burden. We also explored the relationship between urinary catecholamines, cotinine, and electrocardiographic changes. Chapter 3 features the 2 x 2 factorial experimental study designed to compare the acute effects of cigarette smoking and nicotine, with and without a β-blocker (propranolol). We found that chronic cigarette smoking was associated with a shortened PR segment at baseline, and that dopamine possibly mediates this effect. There was also (corrected) QT interval shortening with increased cotinine levels. This experimental study revealed that the non-nicotine constituents in cigarette smoking were mainly responsible for PR segment shortening, through β-adrenoreceptors. Other evidence revealed that, although nicotine in cigarette smoke is primarily responsible for sympathetic activation and (corrected) QT interval shortening, it is the non-nicotine constituents that depress the ST segment. Collectively, acute and chronic exposure studies indicate that smoking may promote cardiac arrhythmia, primarily via β-adrenoreceptors, causing acceleration of dromotropy and ischemia (non-nicotine mediated), and ventricular repolarization (nicotine-mediated). This research elucidated a major physiological mechanism driving the effect of cigarette smoking and nicotine on cardiac electrophysiology. Consequently, these findings will inform U.S. Food and Drug Administration of tobacco and nicotine-containing products’ impact on the human cardiac electrical system, and potentially help regulate alternative forms of nicotine delivery and protect public health