title: Mechanism of exercise hypotension in patients with ischemic heart disease. Role of neurocardiogenically mediated vasodilation.
abstract: BACKGROUND
  Exercise-induced hypotension in patients with coronary artery disease (CAD) has been considered to be due to an inability to achieve an adequate increase in cardiac output to match the demands of exercise. We investigated 10 consecutive patients (9 men and 1 woman; age, 38 to 71 years; mean, 52 years) with angiographically documented CAD and exercise-induced hypotension (EIH) (BPPeak < BPRest). Ten approximately age- and sex-matched patients with documented CAD and normal exercise blood pressure response (NBP) served as control subjects.
  
  
  RESULTS
  Nine patients with EIH and all 10 control subjects underwent forearm plethysmography and radionuclide ventriculography (RNV) during semierect cycle exercise. Forearm vascular resistance (FVR) fell by 35 +/- 21% in exercise-induced hypotension patients versus an increase of 78 +/- 65% in patients with an NBP response (P < .0001). Left ventricular ejection fraction increased by 5.1 +/- 7.5% in the group with EIH versus a fall of 4.1 +/- 6.2% in the control group (P = .004). Cardiac output at peak exercise (RNV) increased by 2.2 +/- 0.89-fold in the group with EIH versus 1.49 +/- 0.47-fold in the control group (P = .04). The tenth patient in the group with EIH underwent invasive hemodynamic evaluation during erect exercise. Systolic blood pressure fell (136/80Rest to 50/40Peak) and cardiac output (Fick) tripled, whereas calculated systemic vascular resistance decreased by a factor of 10. Successful angioplasty to an isolated circumflex lesion resulted in resolution of symptoms and abnormal hemodynamic responses during exercise.
  
  
  CONCLUSIONS
  Abnormal vasodilation associated with a normal or even increased rather than decreased cardiac output response appears to be an important mechanism underlying EIH in some patients with CAD. In the present study, this appears to have been the dominant mechanism in 8 and contributory in 2 of the consecutive patients studied.
authors.affiliation: Department of Cardiology, Australia.
authors.forename: S S
authors.initials: SS
authors.lastname: Lele
authors.forename: G
authors.initials: G
authors.lastname: Scalia
authors.forename: H
authors.initials: H
authors.lastname: Thomson
authors.forename: D
authors.initials: D
authors.lastname: Macfarlane
authors.forename: D
authors.initials: D
authors.lastname: Wilkinson
authors.forename: W
authors.initials: W
authors.lastname: Stafford
authors.forename: F
authors.initials: F
authors.lastname: Khafagi
authors.forename: M
authors.initials: M
authors.lastname: Frenneaux
mesh_terms: D000328:Adult; D000368:Aged; D002302:Cardiac Output; D005260:Female; D005542:Forearm / Q000098:blood supply; D006321:Heart / Q000503:physiopathology; D006801:Humans; D007022:Hypotension / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology; D009420:Nervous System / Q000503:physiopathology; D005082:Physical Exertion; D010991:Plethysmography; D015635:Radionuclide Ventriculography; D013599:Systole; D014664:Vasodilation / Q000502:physiology*