Interventricular vessel of the heart and diuretics

Dear Editor,

I read with interest the review of Roush GC and his colleges concerning diuretics for reducing left ventricular hypertrophy of systemic hypertension.1 No other drug class improves health outcomes with hypertension better than low‐dose thiazides that reduce mortality, stroke, and heart attack. Beta‐blockers and high‐dose thiazides are inferior.2 Natriuretic peptide‐guided treatment of heart failure reduces all‐cause mortality in patients aged <75 years and overall reduces heart failure and cardiovascular hospitalization compared with clinically guided therapy.3 Atrial natriuretic peptide (ANP) is stored mainly in the right atrium and released in response to an increase in atrial distending pressure. Brain natriuretic peptide (BNP) is stored mainly in cardiac ventricular myocardium and may be responsive to changes in ventricular filling pressures.4

In the formation of the fetal muscular part of the interventricular septum (IVS), the expanding ventricles grow and their medial walls approach and fuse, forming the septum. The inside corner between the septum and the right anterior ventricular wall exhibits the deep pits being called interventricular sinuses (ISs). The IS passes through the right IVS formed from the medial wall of the expanding fetal right ventricle (RV). The opening of the interventricular vessel (IV) (kuuselian vessel) is located in the IS between the medial walls of the expanding fetal RV and fetal left ventricle (LV). The IV is not a canal or channel or blood vessel, but a slit between the fibers of the muscle leading to the outer layer of the left central muscular part of the IVS, and runs at an angle of about 90 degrees through the interventricular sphincter (ISP) and the left IVS into the LV. The IV exhibits 2 to 3 oval 2 × 5 mm openings in the left central muscular part of the IVS surrounded by the ISP. Hypoxia may be the physiological factor that recruits IV of the fetal heart and augments the flow of the oxygenated blood from right to left. The ISP and the IV may become patent by relaxing and widening of the helical heart at the right atrial filling phase at the end of the fetal diastole. The sinoatrial node initially activates the right atrium (RA), followed by activation of the left atrium (LA). Left to right communication does not result as the earliest left ventricular activation closes the ISP. Hypoxia may recruit the IV of the heart at the right atrial filling phase and create the venous flow from right to left into the LV. This flow may generate the abnormal fourth heart sound common in hypertrophy of systemic hypertension and in ischemic heart disease. The venous flow moves toward the left outflow tract in the LV.5, 6 The fourth heart sound appears at the 80% submaximal heart rate during a treadmill stress test in normal hearts.7 High heart rate may also cause negative left ventricular pressure and sucking effect at the early diastole of the normal heart.8

I do not yet fully understand the anatomy, function, and embryology of the human heart and circulation. The hypertensive patient with secondary polycythemia of the reference 6 suggests an unusually plentiful venous flow at the right atrial filling phase from right to left through the IV. Currently, I do not have a noninvasive method to recognize the slight venous flow reliably. Venous blood may reach the brain and the coronary arteries during every cardiac cycle. I do not know whether recruitment of the IV by hypoxia or by an increase in right atrial pressure and ANP or BNP is due to fetal physiological reasons.

CONFLICT OF INTEREST

None.