ORONARY ARTERY BYPASS graft (CABG) surgery is one of the most common and costly medical procedures performed in the United States. 1 Its main indications are the relief of angina and improvement in quality of life. 2 Yet as many as half of post-CABG patients report depressive symptoms in the perioperative period, 3 are more likely to experience a decreased healthrelated quality of life (HRQL) and functional status, 4 continued chest pains, 5,6 and inreased rates of rehospitalization and death following CABG surgery independent of cardiac status, medical comorbidity, or the extent of surgery. [7][8][9][10][11] Although the mechanism whereby depression affects post-CABG outcomes remains unknown, 12 widely generalizable strategies to detect and effectively treat post-CABG depression are of great interest. Several treatment trials for depression have been conducted in cardiac populations, but most achieved less than anticipated benefits with regard to reducing mood symptoms [13][14][15][16][17][18][19] or cardiovascular morbidity. [13][14][15][16]19,20 Moreover, none used the proven effective collabo-rative care approach 21 recently recommended by a National Institutes of Health expert consensus panel. 22 Unlike earlier interventions that used a single antidepressant, 13,15,17,18 counseling modality, 20 or antidepressant in combination with counseling for treating cardiacpatientswithdepression, 14,19 collabo-rative care emphasizes a flexible realworld treatment package that involves active follow-up by a nonphysician care manager who adheres to evidence-based Author Affiliations are listed at the end of this article.
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
The relation of abnormal peripheral vascular responses to exercise hypotension confirms the observation of hemodynamic instability in patients with hypertrophic cardiomyopathy. The finding of abnormal vascular responses in patients known to be at increased risk (young age and a family history of hypertrophic cardiomyopathy and sudden death) suggests that hemodynamic mechanisms may be important in the occurrence of sudden death in hypertrophic cardiomyopathy.
Time-domain and spectral measures of HRV yield similar information about the specific autonomic influences on the heart. Global and specific vagal influences on HRV were reduced in patients with symptoms and arrhythmias and global HRV is increased in patients with an adverse family history of HCM, but these indices do not add to the predictive accuracy of established risk factors.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.