LETTER TO THE EDITOR
The enigma of primary pulmonary hypertension
Bernard G. Krohn, MD, FACCa
a 16250 Woodruff Avenue, Bellflower, California 90706-4908, USA
bernardkrohn{at}mediaone.net
Riley et al. (1) observed that exercise increased heart rates and decreased oxygen saturations of arterial hemoglobin abnormally in patients who had primary pulmonary hypertension. They stated that this occurs in subjects with circulatory disease or deconditioning. They did not refer to the studies showing that fast heart rates and desaturation of arterial hemoglobin also occur in well-trained athletes (2,3). They did not measure cardiac outputs in their patients to allow them to calculate stroke volumes, but they concluded that low stroke volume, resulting from pulmonary hypertension, was probably the main factor responsible for the abnormalities that they observed.
The authors showed that the patients, who had primary pulmonary hypertension, worked more slowly, did less work and recovered more slowly than normal subjects. Inhaling nitric oxide reduced the patients’ pulmonary arterial pressures, but changed none of the above abnormal measurements. This made it difficult to claim that the pulmonary hypertension was the cause of the abnormal measurements. The decrease of pulmonary artery pressure after inhalation of nitric oxide and possible, but undemonstrated, increase of blood flow resembled Wilson and Ferraro’s (4) study using hydralazine. This showed that hydralazine decreased arterial pressure and increased cardiac output during exercise in heart failure, but did not influence exercise oxygen consumption or peak lactate concentration or oxygen debt (4). Dilating blood vessels, reducing intravascular pressures and increasing blood flow did not correct the important abnormalities in either situation.
A new clue concerning pulmonary hypertension is in the report of Driss et al. (5) of producing tiny left ventricular infarcts that did not change left ventricular hemodynamics or size, but caused pulmonary hypertension. Riley et al. (1) should extend their studies into the field of neurohumoral and other signaling to improve our understanding of primary pulmonary hypertension.
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References
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- Riley MS, Porszasz J, Engelen MPKJ, Shapiro SM, Brundage BH, Wasserman K. Responses to constant work rate bicycle ergometry exercise in primary pulmonary hypertension: the effect of inhaled nitric oxide. J Am Coll Cardiol. 2000;36:547–556[Abstract/Free Full Text]
- Harms CA, McClaran SR, Nickele GA, Pegelow DF, Nelson WB, Dempsey JA. Effect of exercise-induced arterial O2 desaturation on VO2 max in women. Med Sci Sports Exerc. 2000;32:1101–1108[Medline]
- Powers SK, Lawler J, Dempsey JA, Dodd S, Landry G. Effects of incomplete pulmonary gas exchange on VO2max. J Appl Physiol. 1989;66:2491–2495[Abstract/Free Full Text]
- Wilson JR, Ferraro N. Circulatory improvement after hydralazine or isosorbide dinitrate administration in patients with heart failure: effect on metabolic responses to submaximal exercise. Am J Med. 1981;1:627–633
- Driss AB, Devaux C, Henrion D, et al. Hemodynamic stresses induce endothelial dysfunction and remodeling of pulmonary artery in experimental compensated heart failure. Circulation. 2000;101:2764–2770[Abstract/Free Full Text]
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