Pathophysiology Of Valvular Heart Disease Research Articles

Transcatheter valvular therapies in patients with left ventricular assist devices.

Aortic, mitral and tricuspid valve regurgitation are commonly encountered in patients with continuous-flow left ventricular assist devices (CF-LVADs). These valvular heart conditions either develop prior to CF-LVAD implantation or are induced by the pump itself. They can all have significant detrimental effects on patients' survival and quality of life. With the improved durability of CF-LVADs and the overall rise in their volume of implants, an increasing number of patients will likely require a valvular heart intervention at some point during CF-LVAD therapy. However, these patients are often considered poor reoperative candidates. In this context, percutaneous approaches have emerged as an attractive "off-label" option for this patient population. Recent data show promising results, with high device success rates and rapid symptomatic improvements. However, the occurrence of distinct complications such as device migration, valve thrombosis or hemolysis remain of concern. In this review, we will present the pathophysiology of valvular heart disease in the setting of CF-LVAD support to help us understand the underlying rationale of these potential complications. We will then outline the current recommendations for the management of valvular heart disease in patients with CF-LVAD and discuss their limitations. Lastly, we will summarize the evidence related to transcatheter heart valve interventions in this patient population.

Valvular heart disease and anaesthesia.

Valvular heart disease presents as mixed spectrum lesion in healthcare settings in the third-world and developing countries. Rheumatic heart disease still forms the bulk of the aetiopathology of valve lesions. Mitral and aortic valve lesions top the list of valvular pathology. A thorough understanding of the pathophysiology of valvular heart disease is essential while planning anaesthesia and perioperative care for such patients. Meticulous use of optimal fluids, close monitoring of the changing haemodynamics and avoidance of situations that can cause major reduction of cardiac output and fluid shifts are mandatory to achieve good clinical outcome. We searched MEDLINE using combinations of the following: anaesthesia, aortic, mitral, regurgitation, stenosis and valvular heart disease. We also hand searched textbooks and articles on valvular heart disease and anaesthesia. This article mainly focuses on the understanding the pathophysiology of valvular heart disease in patients presenting for non-cardiac surgeries in secondary and tertiary care setting.

Accurate Assessment of Aortic Stenosis

Aortic valve (AV) stenosis is one of the most common valvular diseases and is the third most common cardiovascular disease in developed countries. It occurs in ≈2.8% of patients ≥75 years of age and can occur because of degenerative calcification and congenital valvular defects such as bicuspid AVs or rheumatic disease.1–3 Calcific aortic stenosis (AS) is associated with increased leaflet stiffness and a narrowed AV orifice, resulting in increased pressure gradients across the valve. The presence of a bicuspid AV significantly increases the risk of AS.4 The natural history of AS is a prolonged asymptomatic period, with progressive reduction of the AV orifice area due to sclerosis initially, culminating in calcific AS. This is accompanied by a corresponding increase in the transaortic pressure gradient (Δ P ) and myocardial pressure overload. Through the preload reserve, the left ventricle (LV) compensates for the increased workload until the sarcomeres stretch to their maximum diastolic length. Once the preload reserve is exhausted, increases in afterload are accompanied by a reduction in stroke volume (SV), resulting in afterload mismatch. Ultimately, this causes LV hypertrophy, associated with an enlargement of cardiac myocytes and increased LV wall thickness.5 Initial diagnosis of AS typically occurs during routine physical examination with the presence of a heart murmur, click, or other abnormal sounds, but undiagnosed patients may experience the onset of severe symptoms such as angina, syncope, and heart failure. Without intervention, patient mortality typically occurs within 5 years of the onset of symptoms.6–11 Multiple studies and reviews have focused on the clinical aspects of this disease, including disease progression, markers of disease severity, treatment guidelines, and outcomes.1–3,6,12–16 Very few reviews have focused on the hemodynamic principles underlying AS and on comparing data obtained across different …

The Year in Cardiology 2012: valvular heart disease

Growth of the ageing population, advances in imaging techniques, newly available percutaneous interventions, and emphasis on the central role of the Heart Team in risk assessment and treatment selection1 combine to place valvular heart disease (VHD) at the centre of developments in cardiovascular medicine and surgery. However, VHD is poorly researched in comparison with other areas of cardiac disease, both at a basic scientific and clinical level. Until recently, there have been virtually no randomized controlled trials and international guidelines are largely based on expert consensus. Principal limitations to quality research are the diverse nature of patients with VHD, inability to identify individuals at the earliest stages of disease, and a lack of financial support and an appropriate investigational infrastructure. Guidelines attempt to address this evidence gap and a key publication this year was the joint European Society of Cardiology (ESC) and European Association of Cardiothoracic Surgeons (EACTS) Guidelines on the Management of VHD.2 This concise and practical document provides recommendations on patient evaluation and risk stratification for both surgical and interventional procedures, coupled with emphasis on multimodality imaging and recommendations from the European Association of Echocardiography on the quantification of valve lesions. Evidence-based implementation of surgical mitral valve repair and transcatheter aortic valve implantation (TAVI) feature strongly together with emphasis on the function of the multidisciplinary Heart Team in achieving optimal outcomes for this challenging group of patients. The pathophysiology of VHD is under-investigated and predictors of disease progression in individual patients poorly understood. Good quality studies examining medical treatment options in early disease are scarce and have been negative to date. Management of asymptomatic patients is therefore challenging and the subject of continuing controversy. Novel imaging strategies examining the relative contributions of valvular calcification and inflammation suggest new therapeutic targets and a means of assessing their …

Imaging modalities in valvular heart disease

Evaluating valvular heart disease requires a multi-parametric analysis of valvular pathology, hemodynamic derangements, and impact on ventricular size and function. The capability to perform real-time three-dimensional (3-D) imaging has vastly strengthened the already established role of echocardiography. CT and MRI advances have led to their use as daily clinical tools. Two-dimensional and 3-D echocardiography and Doppler modalities allow for accurate assessment of valvular lesions, pressure gradients, stenotic valve orifice areas, pulmonary artery pressures, intracardiac pressures, and regurgitant volumes. Quantitation of chamber volumes has become more accurate and reproducible with 3-D echocardiography, CT, and cardiac MRI. Although ultrasound imaging is the primary tool, the other techniques provide adjuvant or alternate options to examine valvular heart disease. This array of imaging modalities is likely to provide greater insights into the pathophysiology of valvular heart disease, new pointers to prognosis, and also guide innovative treatment strategies.

Pathophysiology of valvular heart disease: Implications for nuclear imaging

In general, the echocardiogram has become the mainstay of diagnosis in patients with valvular heart disease. Its strength is that it provides information about valve pathoanatomy and about the severity of stenosis and regurgitation not available by other techniques. However, radionuclide studies offer a more precise gauge of left and right ventricular ejection performance, which is useful in the timing of surgery. Because, at present, most cardiac catheterization procedures in patients with valve disease are performed to evaluate coronary anatomy, a noninvasive technique for detecting coronary disease could obviate the need for invasive studies prior to surgery. The presence of left ventricular hypertrophy especially in aortic stenosis has made myocardial imaging less than perfect in this preoperative evaluation, but clearly this is an area of potential fruitfulness in the use of radionuclide techniques. Additional studies regarding the utility of exercise RNA seem warranted and might be of particular interest in mitral regurgitation, in which little is known about the ability of such studies to help time mitral valve surgery. The addition of estimates of loading during exercise studies is an attractive pathophysiologic adjunct and should be helpful in the interpretation of such studies. The potential role for targeted “hot spot” imaging of ischemia, apoptosis, and necrosis in patients with valvular heart disease remains undefined, although such imaging represents another potential area of investigation that warrants further evaluation.