Abnormal contractile reserve to exercise: a stress echocardiographic abnormality that may be associated with myocardial rather than coronary artery disease.

Abstract

The fundamental principle of stress echocardiography is that left ventricular (LV) abnormalities are usually not apparent in the early stages disease because of the heart’s functional reserve. In the routine interpretation of stress echocardiography, a search for abnormal regional wallmotioniscomplementedbyanassessmentoftheglobalresponse toexercise.ThenormalLVresponsetoexerciseinvolvesanincrement of ejection fraction (EF) and reductions of ventricular volumes, and this information has been used in interpretation from the earliest days of two-dimensional stress echocardiography. 1 Indeed, extensive (usually left main or multivessel) ischemia can cause LV dilatation and reduction of EF. Loss of LV contractile reserve is a more subtle abnormal global LV response, indicating failure of these parameters to improve with exercise rather than to worsen. Typically, this response is defined as a failure to improve EF by >5%, but in addition to assessment of these findings with EF or LV volumes, they have also been defined on the basis of annular excursion, including tissue Doppler. 2 The phenomenon of functional reserve is not limited to systole: the diastolic equivalent of contractile reserve is diastolic reserve. 3 Common causes of impaired contractile reserve include the performance of submaximal exercise and increased ventricular afterload (poorly controlled systemic hypertension 4 or pulmonary hypertension). However, the findings may signify the presence of pathology, including primary myocardial disease, 5,6 or the beginnings of decompensation from regurgitant valve lesions. 7 The possibility of an association between a lack of contractile reserve and overt coronary artery disease has been discounted on the basis that the changes are global rather than regional. What has not been clear is whether the findings might originate from diffuse coronary artery disease. In this issue of the journal, Nasis et al. 8 provide strong evidence that the changes are likely to reflect subclinical myocardial disease rather than coronary disease. In this observational study, 1,134 consecutive patients undergoing treadmill echocardiography underwent invasive angiography or coronary computed tomography. Exclusion of patients with obstructive coronary disease, a hypertensive response, a submaximal heart rate, resting LV impairment, and valvular disease led to a final study group of 332 patients,110 of whom demonstrated abnormal LV contractile reserve, defined by failure to increase EF by >5% with stress. In addition to this response, occurring in the absence of changes on the ‘‘coronary lumenogram,’’ patients with andwithouttheseresponsesdemonstratednodifferencesincoronary microvascular function, as evidenced by myocardial blush grade or Thrombolysis In Myocardial Infarction frame count. These findings allay concerns that the observation of impaired contractile reserve may be a sign of subclinical coronary artery disease. Instead, impaired contractile reserve appears to be a marker of subclinical LV dysfunction. The subgroup of patients without contractile reserve were older, more likely to be female, limited by dyspnea, and more often associated with hypertension, diabetes mellitus, and slightly greater body mass index. These patients also had reduced resting diastolic tissue velocity with increased atrial volumes. Their higher heart rate responses may reflect abnormal sympathetic activation, as proposed by the authors, or may simply reflect lesser levels of physical fitness and the need for greater heart rate to compensate for relatively lower stroke volume. Two aspects of this observation are of particular interest. First, this response is clearly afterload dependent. The authors removed patients with hypertensive responses to exercise, but as their definition of this entity was a systolic blood pressure >210 mm Hg in men and >190 mm Hg in women, these exclusions represent the most extreme manifestation of this problem. Indeed, despite the exclusion of overt hypertensive responses to exercise, arterial elastance was more abnormal in patients lacking contractile reserve. 8 This balance between peak systolic pressure and end-systolic volume has been the source of an often neglected body of work in the stress echocardiography literature, 9 with some studies showing events to be associated with failure to increase the ratio between blood pressure and end-systolic volumes. 10