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Cardiovascular Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The different types of diastolic murmur are as follows: Early diastolic murmur: This is a decrescendo murmur in diastole that occurs immediately after the second heart sound. It is caused by aortic or pulmonary regurgitation.Mid-late diastolic murmur: A low-frequency rumble is only heard at the apex and often follows an opening snap (OS). It is due to either MS or tricuspid stenosis.
Arterial Pressure Waveform Analysis
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Valuable indices of ventricular–vascular interaction can be determined from separation of the aortic wave into systolic and diastolic periods. Tension time index (Sarnoff et al., 1958; Braunwald, 1997a) is the integral of pressure and time during systole and is an index of left ventricular myocar-dial oxygen and blood demand. The diastolic time index is the integral of pressure and time during diastole and is an index of capacity for left ventricular perfusion through the coronary arteries (Feigl, 1983; Nichols and O'Rourke, 1990; O'Rourke et al., 1992c). Subendocardial viability ratio (Chapter 14) is the ratio of diastolic time index to tension time index and is a measure of the propensity for myocardial ischemia on the basis of altered hemodynamic forces (Buckberg et al., 1972a, 1972b, 2008; Hoffman and Buckberg, 1978; O'Rourke, 1982b; Braunwald, 1997a). Subendocardial ischemia has been shown to occur even when coronary arteries are patent when this index falls below 0.7 (Buckberg et al., 1972a). Mean diastolic pressure is another measure of the capacity for coronary perfusion (Figure 14.13) (O'Rourke, 1982b; Nichols and O'Rourke, 1990), while both mean aortic systolic pressure and endsystolic pressure have been taken as indices of left ventricular systolic load (Weber and Janicki, 1971; Suga and Sagawa, 1974).
Venous flow is pulsatile
Published in Dinker B. Rai, Mechanical Function of the Atrial Diastole, 2022
When the ventricle contracts it surges a volume of blood into the great arteries. The arteries expand as a result of this volume of blood which can be manually felt and visually observed. We have termed this phenomenon the arterial pulse. Historically, in the circulatory system the contraction of the heart or of the vessels was named “systole” and the dilatation or filling phase was called “diastole.” The term diastole was also applied to the pulsation of the arteries during that phase. Currently the terms systole and diastole are restricted to the description of the atria and ventricles of the heart. Dilatation or diastole of the artery is now termed “pulsation.” However, the age-old theory that the systole is the only active phase of the heart remains unchanged. The diastole is always considered to be the resting phase, wherein the supplying of the cardiac chambers with blood occurs during this phase.
Association of physical activity and trajectories of physical activity with cardiovascular disease
Published in Expert Review of Cardiovascular Therapy, 2023
Steven G. Chrysant, George S. Chrysant
Among the many CV benefits of exercise are its beneficial effects on cardiac remodeling through the changes in structure, cardiac size, cardiac mass, geometry, and function in young and old hearts [107]. The heart undergoes several morphological and functional changes with age, such as LVH, increased myocyte cell size, and decreased ventricular size [108–110]. Autopsies of the human heart show higher deposits of collagen in subjects older than 65 years compared to younger subjects 20–25 years of age, even without underlying cardiac disease [111]. Similar changes in cardiac morphology have also been noted in experimental animals [112]. These structural changes of the heart are associated with diastolic dysfunction with impaired relaxation and diminished ability to respond to cardiac work due to diminished inotropic and chronotropic reserve [110]. The increased cardiac size in athletes with increased atrial and left ventricular size and volume, is of the so-called, physiological type and not associated with myocardial dysfunction [113]. Clinical evidence also, suggests that exercise-induced cardiac hypertrophy increases the systolic function of the heart in previously sedentary subjects and improves their aerobic exercise performance [114,115]. The long-term benefits of exercise have been attributed to its multiple clinical and molecular cardiac adaptations associated with improvement in the quality of life and prolongation of life span [116,117].
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).
Complications associated with myocardial bridging in four children without underlying cardiac disease: a case series
Published in Paediatrics and International Child Health, 2021
Federica Brancato, Donato Rigante, Marco Piastra, Alessandro Gambacorta, Claudia Aurilia, Gabriella De Rosa
One of the most important triggers of symptomatic MB is intense physical activity which through tachycardia and increased contractility can facilitate myocardial ischaemia. During tachycardia, systole occupies a greater proportion of the cardiac cycle because of shortening of the diastolic filling period. Other pathophysiological factors that might reveal or exacerbate MB are age, left ventricular hypertrophy and coronary atherosclerosis, since all of these may worsen the supply-demand mismatch imposed by the bridge, reducing the coronary reserve [15]. Symptomatic patients may also present with clinical manifestations of myocardial ischaemia such as acute coronary syndrome, coronary spasm, exercise-induced dysrhythmias, myocardial stunning, transient ventricular dysfunction and syncope [15]. Only patients with symptomatic MB or those with objective signs of ischaemia require treatment. In most cases, beta-blockers, ivabradine and calcium channel blockers are effective in reducing symptoms [15]. In adults, myotomy, coronary artery by-pass surgery and stenting may be used to improve symptoms in patients with MB who are refractory to medical therapy [2,20,22,23]. MB is diagnosed by coronary or CT angiography, but it is sometimes established intra-operatively or at post-mortem examination. Another relevant diagnostic test is the stress ECG: the main objective of stress testing for myocardial ischaemia is to demonstrate the mismatch between myocardial oxygen demand and myocardial perfusion [22].