The Role of Vessel Tone in Maintaining Pulmonary Vascular Resistance in Patients with Mitral Stenosis

Abstract

Changes in pulmonary vascular (arteriolar) resistance were estimated in 58 patients with mitral stenosis following mitral valvotoimny and during exercise. Evidence is presented that changes in "resistance" reflect active changes in the caliber of the vessels due to alteration in their smooth muscle tone, valvotonmy being followed by a decrease in tone and exercise by an increase.I T IS well known that patients with mitral stenosis have medial hypertrophy of the pulmonary arteries, that a muscular media develops in the arterioles,1-4 and that these histologic changes often are accompanied by an increased resistance to blood flow through the vessels of the lungs.5 Many attempts have been made to define the mechanism of this increased resistance with the use of adrenergic and ganglionic blocking agents.6-9 The conflicting nature of the conclusions emphasizes the difficulty in interpreting the results. This is mainly due to the fact that the potent action of these drugs on the systemic circulation makes it difficult to decide whether the changes in the pulmonary circulation are actively or passively induced. The recent use of acetylcholine injected into the pulmonary artery in such a concentration that it is inactivated before reaching the left side of the heart has demonstrated that the high pulmonary vascular resistance in mitral stenosis is at least partly functional;10 that is, tone is present in the smooth muscle of the pulmonary vessels and this contributes to the pulmonary hypertension.In the present paper, some of the factors are examined that may be concerned in the maintenance of this tone. METHODSThe hemodynamic data on 58 adult patients were analyzed. All clinical and laboratory findings, and this was confirmed in the majority of eases at the time of mitral valvotoiny. There were 42 women and 16 men, aged 18 to 53 years, with an average age of 34 years for the women and 38 years for the men. Any patient having a systemic blood pressure higher than 140 mm. Hg systolic and 90 mm. diastolic was not included in this report. Intravascular pressures were recorded by straingage manometers, the zero reference point being midehest at the level of the third interspace on the sternum with the patient supine. The cardiac output was determined by the Fick principle. The rate of consumption of oxygen was measured by collecting expired air for 5 minutes and analyzing it immediately by the Haldane method; blood samples from the pulmonary and radial arteries withdrawn midway during the collection of expired air were analyzed for their oxygen content in duplicate by the method of Van Slyke and Neill.1"The oxygen capacity of hemoglobin was measured by the method of Sendroy,12 with the modification of Roughton, Darling, and Root.13 Midway during the collection of the blood samples, a record of pulmonary and radial artery pressures was obtained that was considered to represent the resting state. The catheter tip was then advanced into the "wedge" position of either peripheral lung field and the pressure was measured.For th...

Brisket Disease. Iii. Spontaneous Remission of Pulmonary Hypertension and Recovery From Heart Failure*

“…On this basis, regression of pulmonary hypertension in brisket disease noted in the present study would depend primarily on lowering of left ventricular filling pressure. Again, this would be analogous to the situation that obtains in certain patients with mitral stenosis when the valvular obstruction is relieved surgically (10)(11)(12).…”

World Health Organization Pulmonary Hypertension Group 2: Pulmonary hypertension due to left heart disease in the adult—a summary statement from the Pulmonary Hypertension Council of the International Society for Heart and Lung Transplantation

“…In a series of 300 patients, Wood observed severe pre-capillary PH (PVR Ͼ 6 WU) complicating mitral stenosis in 26% of patients. 37 In isolated mitral regurgitation with preserved LVEF, 17% of patients had PA systolic pressure (PASP) Ͼ 70 mm Hg 38 and 76% had PASP Ͼ 30 mm Hg. Schwammenthal et al 39 showed that elevated PAP at rest and during exercise in mitral stenosis is related to a greater extent to net atrioventricular compliance than mitral valve area.…”

Saudi Guidelines on the Diagnosis and Treatment of Pulmonary Hypertension: Pulmonary hypertension due to left heart disease

“…[2] Historically, mitral valve disease has probably been the best-described cause of PH. [34] In the current era, heart failure is recognized as the predominant cause of elevated left-sided filling pressures resulting in PH. [5] Despite the high prevalence of WHO Group 2 PH, the major focus of research on PH over the past decade has been on WHO Group 1 pulmonary arterial hypertension (PAH).…”