Effects of altitude on exercise level and heart rate in patients with coronary artery disease and healthy controls.

Background. To evaluate the safety and effects of high altitude on exercise level and heart rate in patients with coronary artery disease compared with healthy controls.Methods. Eight patients with a history of an acute myocardial infarction (ejection fraction >5%) with a low-risk score were compared with seven healthy subjects during the Dutch Heart Expedition at the Aconcagua in Argentina in March 2007. All subjects underwent a maximum exercise test with a cycle ergometer at sea level and base camp, after ten days of acclimatisation, at an altitude of 4200 m. Exercise capacity and maximum heart rate were compared between groups and within subjects.Results. There was a significant decrease in maximum heart rate at high altitude compared with sea level in both the patient and the control group (166 vs. 139 beats/min, p<0.001 and 181 vs. 150 beats/min, p<0.001). There was no significant difference in the decrease of the exercise level and maximum heart rate between patients and healthy controls (-31 vs. -30%, p=0.673).Conclusion. Both patients and healthy controls showed a similar decrease in exercise capacity and maximum heart rate at 4200 m compared with sea level, suggesting that patients with a history of coronary artery disease may tolerate stay and exercise at high altitude similarly to healthy controls. (Neth Heart J 2010;18:118-21.).

Impact of high altitude on echocardiographically determined cardiac morphology and function in patients with coronary artery disease and healthy controls.

AIMS: To evaluate the impact of high altitude on cardiac morphology and function in patients with coronary artery disease (CAD) and healthy controls. METHODS AND RESULTS: Eight patients with a history of acute myocardial infarction [53 +/- 8 years, left ventricular (LV) ejection fraction 54 +/- 6%] and a low risk score were compared with seven healthy controls (41 +/- 16 years) during the Dutch Heart Expedition 2007 at the Aconcagua (6960 m) in Argentina. An exercise test and echocardiography were performed at sea level and at base camp (4200 m). In the apical four-chamber view, right ventricular (RV) diameter, tricuspid annular plane systolic excursion (TAPSE), early transmitral inflow peak velocity (E), atrial transmitral inflow peak velocity (A), and peak tissue velocity during early diastole (E') were obtained. Changes in global LV function and wall motion score index (WMSI) were used as markers of ischaemia. There were no significant differences in individual global LV function and WMSI at high altitude compared with sea level in both groups. A significant increase in RV diameter was observed in the patient group at 4200 m compared with sea level and a trend towards the same result in the control group. A decrease in TAPSE was observed. Measurements of the E' showed a significant decrease in the LV septum and lateral wall at high altitude compared with sea level in both groups. CONCLUSION: Symptoms and echocardiographic signs of myocardial ischaemia were absent in low-risk patients with a history of CAD during and after exercise up to an altitude of 4200 m. Patients and healthy controls showed comparable changes at high altitude compared with sea level with an increase in RV diameter, a decrease in TAPSE, and decreased E' as early signs of pulmonary hypertension and LV diastolic dysfunction. As these alterations are most likely physiological adaptation to high altitude, the results seem to affirm current guidelines. The safety of expanding previous recommendations to patients with low-risk CAD to an altitude ascent of 4200 m requires confirmation in a larger study with appropriately defined clinical endpoints.

The effect of heart rate on the membrane responsiveness of rabbit atrial muscle.

The maximum rate of rise of action potentials in myocardial fibers of the rabbit atrium decreases with an increase in heart rate. This decrease of the dV/dt max is accompanied by a decrease of the diastolic transmembrane potential prior to the moment of activation (take-off potential). Comparison of the membrane responsiveness curve (relation between dV/dt max and take-off potential) as measured by varying the extracellular potassium concentration at a fixed rate of stimulation, with the effect of changes in the frequency of stimulation on dV/dt max and take-off potential made clear that the fall in dV/dt max after a sudden increase in heart rate was stronger than could be explained by the concomitant decrease of the take-off potential alone. This implicates that the membrane responsiveness itself is heart rate dependent. A possible explanation for this observation is that when heart rate is increased the active Na/K pump is not able to maintain the intracellular concentration of Na and K at the original level. Acceleration of the heart will lead to an intracellular loss of potassium and a gain of sodium. The first causes a diminishment of the diastolic membrane potential which according to the membrane responsiveness curve is attended with a decrease of the dV/dt max. The second results in a decrease of the sodium concentration gradient and therefore in a further reduction of the dV/dt max. This hypothesis was confirmed by experiments with ouabain added to the perfusion fluid. Ouabain, which is known to inhibit the Na/K pump, caused a decrease of both the take-off potential and dV/dt max that was completely comparable with the effects of an increase of the frequency of stimulation. In addition, observation of the time course of the changes in dV/dt max and membrane "resting" potential after a sudden change in the rate of stimulation, gave support to the electrogenic concept of the active Na/K pump in cardiac muscle.