Cardiopulmonary exercise testing (CPET) is a well-accepted physiologic evaluation technique in patients diagnosed with heart failure and in individuals presenting with unexplained dyspnea on exertion. Several variables obtained during CPET, including oxygen consumption relative to heart rate (VO 2 /HR or O 2 -pulse) and work rate (VO 2 /Watt) provide consistent, quantitative patterns of abnormal physiologic responses to graded exercise when left ventricular dysfunction is caused by myocardial ischemia. This concept paper describes both the methodology and clinical application of CPET associated with myocardial ischemia. Initial evidence indicates left ventricular dysfunction induced by myocardial ischemia may be accurately detected by an abnormal CPET response. CPET testing may complement current non-invasive testing modalities that elicit inducible ischemia. It provides a physiologic quantification of the work rate, heart rate and O 2 uptake at which myocardial ischemia develops. In conclusion, the potential value of adding CPET with gas exchange measurements is likely to be of great value in diagnosing and quantifying both overt and occult myocardial ischemia and its reversibility with treatment.

Purpose of reviewThere is growing clinical interest for the use of cardiopulmonary exercise testing (CPET) to evaluate patients with or suspected coronary artery disease (CAD). With mounting evidence, this concise review with relevant teaching cases helps to illustrate how to integrate CPET data into real world patient care.Recent findingsCPET provides a novel and purely physiological basis to identify cardiac dysfunction in symptomatic patients with both obstructive-CAD and nonobstructive-CAD (NO-CAD). In many cases, abnormal cardiac response on CPET may be the only objective evidence of potentially undertreated ischemic heart disease. When symptomatic patients have NO-CAD on coronary angiogram, they are still at increased risk for cardiovascular events. This problem appears to be more common in women than men and may warrant more aggressive risk factor modification. As the main intervention is lifestyle (diet, smoking cessation, exercise) and medical therapy (statins, angiotensin-converting enzyme inhibitors, beta-blockers), serial CPET testing enables close surveillance of cardiovascular function and is responsive to clinical status.SummaryCPET can enhance outpatient evaluation and management of CAD. Diagnostically, it can help to identify physiologically significant obstructive-CAD and NO-CAD in patients with normal routine cardiac testing. CPET may be of particular value in symptomatic women with NO-CAD. Prognostically, precise quantification of improvements in exercise capacity may help to improve long-term lifestyle and medication adherence for this chronic condition.

Abnormal heart-rate response during CPET is more effective than stress ECG for identifying under-treated atherosclerosis and may be of utility to identify cardiac dysfunction in symptomatic patients with normal routine cardiac testing.

Evidence demonstrating the potential value of cardiopulmonary exercise testing (CPET) to accurately detect myocardial ischemia secondary to macro-vascular disease is beginning to emerge. Despite distinct mechanisms mediating ischemia in micro-vascular and macrovascular coronary artery disease (CAD), the net physiologic effect of exercise-induced left ventricular (LV) dysfunction is common to both. The abnormal physiologic response to CPET may, therefore, be similar in patients with macro-and micro-vascular ischemia. The following case report describes the CPET abnormalities in a patient with suspected microvascular CAD and the subsequent improvement in LV function following three weeks of medical therapy with the anti-ischemic drug ranolazine.

Key markers of ventilatory efficiency and (Equation is included in full-text article.)O2 kinetics during CPX significantly improve following CR. Expanding the list of variables assessed via CPX may provide better resolution in validation of CR therapeutic efficacy in patients with CAD.