China
Africa
Explore chapters and articles related to this topic
Valve Disease
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Supravalvar aortic stenosis is the least common type of left ventricular outflow obstruction (seeFig. 3.29a) and most patients with this condition have Williams syndrome. Williams syndrome is also known as idiopathic infantile hypercalcaemia and patients go on to develop renal calcification. It is a rare multi-system genomic disorder, caused by 7q11.23 microdeletion with a prevalence of 1/7500–1/20 000 live births. Virtually all cases have mental retardation, with characteristic elfin-type faces. There is disordered mosaic architecture in the elastic tissue of the aortic media giving rise to a hypoplastic thickened aorta with congenital supravalvar aortic stenosis. The lesion may be present as a discrete shelf, as a so-called hour-glass deformity or as a tubular variety in which most of the aortic arch and its branches are thickened, which is the rarest. The coronary arteries arise from the segment under high pressure and this causes them to become dilated and tortuous with early onset of atherosclerosis. This, in combination with left ventricular hypertrophy is responsible for sudden deaths in this condition. Mortality is highest in patients with multilevel obstruction.
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
HFpEF refers to a failure of diastolic function; the heart is unable to adequately fill with blood during diastole, but is still able to eject a good proportion of this reduced amount as stroke volume. HFpEF can be due to: Stenosis of the mitral or tricuspid valve, preventing blood from flowing into the ventricle during diastole.Changes in the compliance (or distensibility) of the ventricular myocardium, so that it does not expand as the ventricle fills with blood. A poorly compliant ventricle will have a reduced volume of blood at the end of diastole, and therefore will eject a smaller amount during systole, leading to a reduced cardiac output.Ventricular hypertrophy may occur in response to some heart problems; the ventricular wall becomes thicker and less compliant. Hypertrophy can occur in patients with a history of hypertension, valve problems and/or renal failure, as the myocardium adapts to increased stress on the ventricular wall.
Ion Transport and Left Ventricular Hypertrophy in Essential Hypertension
Published in Antonio Coca, Ricardo P. Garay, Ionic Transport in Hypertension: New Perspectives, 2019
Antonio Coca, Alejandro De la Sierra, Alvaro Urbano-Márquez
The Framingham Heart Study showed that essential hypertensives with definite electrocardiographic signs of LVH increased from three- to tenfold their mortality rates due to all cardiovascular diseases with respect to hypertensives without signs of cardiac hypertrophy. Of particular interest was the demonstration of a negative prognostic value of LVH even after adjustment for the severity of hypertension, which lends LVH the character of independent risk factor. Ventricular hypertrophy is a dynamic process that can develop and reverse in a period of a few weeks, both in experimental hypertension and clinical practice. Thus, contrary to the classic notion LVH seems not to be a late and irreversible pressure-related complication of EH, but an early phenomenon subject to a dynamic modification in the evolution of the disease.
Metformin: evidence from preclinical and clinical studies for potential novel applications in cardiovascular disease
Published in Expert Opinion on Investigational Drugs, 2023
Adel Dihoum, Graham Rena, Ewan R Pearson, Chim C Lang, Ify R Mordi
Left ventricular hypertrophy is a key risk factor for development of heart failure and is associated with an increased risk of adverse cardiovascular outcome [50]. Regression of LVH using antihypertensive therapy is associated with a reduction in adverse cardiovascular events [51,52]. Metformin may reduce cardiac remodeling and hypertrophy via different mechanisms. Metformin reduces myocardial fibrosis and collagen synthesis, which is an important pathophysiological process that increases myocardial stiffness, reducing pumping capacity, and contributes to heart failure [19]. Metformin can inhibit the TGF-β1–Smad3 signaling pathway [53], which plays a critical role in the fibrotic remodeling of the infarcted ventricle [54]. Metformin’s effects on KLF-15 may also play an important role in its effects on LVH [55].
Anti-hypertensive effects of Callisia fragrans extract on Reno-vascular hypertensive rats
Published in Clinical and Experimental Hypertension, 2022
Xoan Thi Le, Loan Thanh Thi Nguyen, Phuong Thi Nguyen, Tai Van Nguyen, Hiep Van Nguyen, Hang Thi Nguyet Pham, Hong Nguyen Tran, Thang Dac Hoang, Dong Van Le, Kinzo Matsumoto
Administration of C. fragrans extract (500 mg/kg) as well as captopril (20 mg/kg) significantly mitigated the increase in the heart weight, body weight ratio, and left ventricular wall thickness caused in the 2K1C model rats. The prevention of myocardial hypertrophy is one of the major endpoints in the treatment of hypertension since long-term hypertension induces left ventricular hypertrophy, a risk factor for coronary heart disease, congestive heart failure, ventricular arrhythmia, and sudden death (17). Angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics reportedly reduce the left ventricular mass, whereas alpha-adrenergic blockers and direct-acting vasodilators do not exhibit the effect on myocardial hypertrophy (17). Thus, although the suppressive effect of C. fragans on the left ventricular hypertrophy observed in reno-vascular hypertensive rats was less potent than that of captopril, the present results suggest that C. fragans possesses a beneficial effect on the cardiovascular system besides blood pressure-lowering activity.
Physiological characterization of an arginine vasopressin rat model of preeclampsia
Published in Systems Biology in Reproductive Medicine, 2022
Sapna Ramdin, Thajasvarie Naicker, Virushka Pillay, Sanil D. Singh, Sooraj Baijnath, Blessing N Mkhwanazi, Nalini Govender
Earlier studies also linked AVP to arterial blood pressure regulation (Jablonskis and Howe 1993; Song and Martin 2006; Li et al. 2012). The elevations in both systolic and diastolic blood pressure in our study throughout pregnancy in the PAVP group, suggests that arginine vasopressin stimulates the renin-angiotensin aldosterone system (RAAS). This results in vasoconstriction, which is mediated via the V1a receptor and consequently increases peripheral resistance and systemic blood pressure as observed in our study (Qian 2018). Myocardial atrial contraction results in an atrial-induced increase in end-diastolic pressure, which subsequently enhances ventricular contraction. Arginine vasopressin increases the impact of norepinephrine and Ang II on cardiac muscle and blood vessels thus altering hemodynamic function (Lee et al. 2003), and negatively affects myocardial contraction (Goldsmith 2005; Goldsmith and Gheorghiade 2005). Chronic hypertension results in diastolic dysfunction and consequent left ventricular hypertrophy thereby reducing cardiac compliance (Lorell and Carabello 2000). This results in a higher diastolic pressure–volume relationship where even minor elevations in left ventricular end-diastolic volume induces a significant rise in left ventricular end diastolic pressure (Gutierrez and Blanchard 2004). The pronounced effect of AVP on diastolic pressure may be due to the exaggerated interaction of AVP with the V1A and V2 receptors on peripheral blood vessels (Goldsmith 2005; Goldsmith and Gheorghiade 2005).