The percentage of blood that regurgitates back through the aortic valve due to AR is known as the regurgitant fraction. This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta, and therefore an increase in the pulse pressure. Since some of the blood that is ejected during systole regurgitates back into the left ventricle during diastole, there is decreased effective forward flow in AR.While diastolic blood pressure is diminished and the pulse pressure widens, systolic blood pressure generally remains normal or can even be slightly elevated, this is because sympathetic nervous system and the renin-angiotensin-aldosterone axis of the kidneys compensate for the decreased cardiac output. Catecholamines will increase the heart rate and increase the strength of ventricular contraction, directly increasing cardiac output. Catecholamines will also cause peripheral vasoconstriction, which causes increased systemic vascular resistance and ensures that organs are adequately perfused. Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II. In the case of chronic aortic  with resultant cardiac remodeling, heart failure will develop, and it is possible to see systolic pressures diminish. Aortic regurgitation causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.The volume overload, due to elevated pulse pressure and the systemic effects of neuroendocrine hormones causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI.
Hereditary xerocytosis occurs more commonly in African populations, and it exhibits complex interactions with other hereditary alterations of red blood cells, including sickle cell disease and malaria resistance.Osmosis leads to the red blood cell having a constant tendency to swell and burst. This tendency is countered by manipulating the flow of sodium and potassium ions. A pump forces sodium out of the cell and potassium in, and this action is balanced by a process called the passive leak. In overhydrated hereditary stomatocytoses, the passive leak is increased and the erythrocyte becomes swamped with salt and water. The affected erythrocytes have increased osmotic fragility. Haemolytic anaemia results. For as yet unknown reasons, the cells take on the shape of a cup, with a mouth-shaped (stoma) area of central pallor. Overhydrated hereditary stomatocytosis is frequently linked to mutations in genes that encode components of the band 3 complex, such as RHAG. It is the altered band 3 protein complex which mediates the cation leaks that are characteristic of hydrocytotic hereditary stomatocytosis.Rare cases of hereditary spherocytosis can occur without cation leaks. These include cases of phytosterolemia nonleaky stomatocytosis, a disorder of lipid metabolism associated with mutations in ABCG5 and/or ABCG8, which encode sterol transporters. The resulting abnormal sterol composition of erythrocyte cell membranes causes them to appear as deformed stomatocytes on peripheral blood smear. Diagnosis
Ektacytometry may be helpful in distinguishing different subtypes of hereditary stomatocytosis. Variants
Haematologists have identified a number of variants. These can be classified as below.