Abnormal blood pressure response during exercise in hypertrophic cardiomyopathy.

Abstract

To investigate the incidence of abnormal exercise blood pressure responses in hypertrophic cardiomyopathy (HCM) and the potential role of hemodynamic instability as a mechanism of sudden death, 129 consecutive patients with HCM underwent maximal symptom-limited treadmill exercise testing with blood pressure recording. Four patterns of blood pressure response were observed. Forty-three patients had significant exercise hypotension, with either a continuous fall in systolic blood pressure (n=5) from the start of exercise or a sudden fall in systolic blood pressure (20-100 mm Hg; mean, 40 mm Hg) from the peak value (n =38), 23 patients had a normal response during exercise but an abnormal blood pressure response in the recovery period, and the remaining 62 patients demonstrated a normal blood pressure response. Patients with exercise hypotension were younger (33±14 versus 46±14 years) and more of them had a family history of HCM and sudden death compared with those with a normal blood pressure response (15 of 43 versus 6 of 62 patients). Similarly, the 23 patients with abnormal recovery blood pressure responses were younger (43±+16 versus 46±+14 years) and had a higher incidence of a family history of sudden death (10 of 24 versus 6 of 62 patients). Left ventricular cavity dimensions were smaller in those with exercise hypotension, but 11 other clinical, echocardiographic, and arrhythmic variables were similar. To assess the mechanism of exercise hypotension, 14 patients who demonstrated exercise hypotension and 14 symptomatic patients with a normal exercise blood pressure response underwent invasive hemodynamic exercise testing. In the hypotensive group, cardiac index increased from 2.6 to 9.5 1/min/m2 at peak exercise similar to the increase found in patients with a normal blood pressure response. Cardiac index at peak exercise was marginally higher in the hypotensive group at peak exercise. Systemic vascular resistance was similar at rest and after 2 minutes of exercise, but resistance was significantly lower in the hypotensive group at peak exercise (428±185 versus 744±187 dynes/sec/cm-5; p=0.0001). Exercise hypotension is common in HCM (33%) and is due to a fall in systemic vascular resistance occurring despite a rising cardiac index. The association of hemodynamic instability, young age, and an adverse family history emphasizes the potential role of hemodynamic collapse as an initiating mechanism of sudden death in HCM. Prospective evaluation, particularly of young patients, is warranted. (Circulation 1990;82:1995-2002 Sudden death is common in hypertrophic cardiomyopathy (HCM

Response of the Stroke Volume and Blood Pressure of Young Patients With Nonobstructive Hypertrophic Cardiomyopathy to Exercise

“…Frenneaux et al found that during exercise, the blood pressure fell in 33% of the HCM patients, and an abnormal blood pressure response during the recovery after exercise was observed in 23% of the patients. 5 These abnormal pressure responses are responsible for the poor prognosis of these patients, 7,8,13 and that they are frequently seen in young individuals with HCM. 5 However, it seems that these pressure depressions are independent of the increase in CO. 5 On the other hand, Lele, et al 14 reported that HCM patients show an insufficient increase in CO during exercise, as measured by equilibrium radionuclide ventriculography, and that the exercise capacity correlated with both the peak cardiac index 14,15 and peak stroke index.…”

“…[1][2][3][4] Despite the lack of an association with arrhythmias, 4 sudden cardiac death is more likely to occur in young patients than adult patients with HCM and the reason for this is unclear, although it was recently suggested that exercise-induced hypotension is related to sudden cardiac death in HCM patients. [5][6][7][8] The aim of the present study was to measure the cardiac output (CO) of young patients with HCM during exercise using impedance plethysmocardiography to elucidate the hemodynamic response of these patients to exercise.…”

Hemodynamic changes and prognosis in patients with hypertrophic cardiomyopathy and abnormal blood pressure responses during exercise

“…According to the previous reports, the mechanism of abnormal BPR was explained as follows: (1) An inappropriate fall in SVR caused by an excessive peripheral vasodilatation led to a centrally mediated reflex by ventricular baroreceptor stimulation, resulting in an inhibition of sympathetic tone in resistant vessels; 9,10,18 (2) there was an inappropriate increase in stroke volume due to impaired LV filling secondary to LV hypertrophy and tachycardia. 19 Olivotto et al speculated that the mechanism of abnormal BPR during exercise may be different according to the age; that is, abnormal BPR may reflect hemodynamic instability in young patients (< 50 years), while in older patients (≥ 50 years) it may simply reflect age-related cardiovascular changes that have little prognostic relevance.…”

“…[7][8][9] Furthermore, the literature suggests that abnormal BPR is caused by an inappropriate decrease in systemic vascular resistance (SVR), 9,10 and subendocardial ischemia. 11 On the other hand, we previously reported that some patients with nonobstructive HCM showed systolic dysfunction during exercise.…”

Systolic Dysfunction and Blood Pressure Responses to Supine Exercise in Patients With Hypertrophic Cardiomyopathy

“…[3][4][5] The possible mechanisms responsible for these abnormalities are thought to include an abnormal decrease in systemic vascular resistance 3,4 and subendocardial ischemia. 5 We have reported previously that some patients with non-obstructive HCM show a decrease in ejection fraction (EF) during exercise.…”