E xercise testing remains a remarkably durable and versatile tool that provides valuable diagnostic and prognostic information regarding patients with cardiovascular and pulmonary disease. Exercise testing has been available for more than a half century and, like many other cardiovascular procedures, has evolved in its technology and scope. When combined with exercise testing, adjunctive imaging modalities offer greater diagnostic accuracy, additional information regarding cardiac structure and function, and additional prognostic information. Similarly, the addition of ventilatory gas exchange measurements during exercise testing provides a wide array of unique and clinically useful incremental information that heretofore has been poorly understood and underutilized by the practicing clinician. The reasons for this are many and include the requirement for additional equipment (cardiopulmonary exercise testing [CPX] systems), personnel who are proficient in the administration and interpretation of these tests, limited or absence of training of cardiovascular specialists and limited training by pulmonary specialists in this technique, and the lack of understanding of the value of CPX by practicing clinicians.Modern CPX systems allow for the analysis of gas exchange at rest, during exercise, and during recovery and yield breath-by-breath measures of oxygen uptake (V O 2 ), carbon dioxide output (V CO 2 ), and ventilation (V E). These advanced computerized systems provide both simple and complex analyses of these data that are easy to retrieve and store, which makes CPX available for widespread use. These data can be readily integrated with standard variables measured during exercise testing, including heart rate, blood pressure, work rate, electrocardiography findings, and symptoms, to provide a comprehensive assessment of exercise tolerance and exercise responses. CPX can even be performed with adjunctive imaging modalities for additional diagnostic assessment. Hence, CPX offers the clinician the ability to obtain a wealth of information beyond standard exercise electrocardiography testing that when appropriately applied and interpreted can assist in the management of complex cardiovascular and pulmonary disease.

Making a firm diagnosis of chronic heart failure with preserved ejection fraction (HFpEF) remains a challenge. We recommend a new stepwise diagnostic process, the ‘HFA–PEFF diagnostic algorithm’. Step 1 (P=Pre-test assessment) is typically performed in the ambulatory setting and includes assessment for HF symptoms and signs, typical clinical demographics (obesity, hypertension, diabetes mellitus, elderly, atrial fibrillation), and diagnostic laboratory tests, electrocardiogram, and echocardiography. In the absence of overt non-cardiac causes of breathlessness, HFpEF can be suspected if there is a normal left ventricular ejection fraction, no significant heart valve disease or cardiac ischaemia, and at least one typical risk factor. Elevated natriuretic peptides support, but normal levels do not exclude a diagnosis of HFpEF. The second step (E: Echocardiography and Natriuretic Peptide Score) requires comprehensive echocardiography and is typically performed by a cardiologist. Measures include mitral annular early diastolic velocity (e′), left ventricular (LV) filling pressure estimated using E/e′, left atrial volume index, LV mass index, LV relative wall thickness, tricuspid regurgitation velocity, LV global longitudinal systolic strain, and serum natriuretic peptide levels. Major (2 points) and Minor (1 point) criteria were defined from these measures. A score ≥5 points implies definite HFpEF; ≤1 point makes HFpEF unlikely. An intermediate score (2–4 points) implies diagnostic uncertainty, in which case Step 3 (F1: Functional testing) is recommended with echocardiographic or invasive haemodynamic exercise stress tests. Step 4 (F2: Final aetiology) is recommended to establish a possible specific cause of HFpEF or alternative explanations. Further research is needed for a better classification of HFpEF.

Making a firm diagnosis of chronic heart failure with preserved ejection fraction (HFpEF) remains a challenge. We recommend a new stepwise diagnostic process, the ‘HFA–PEFF diagnostic algorithm’. Step 1 (P=Pre‐test assessment) is typically performed in the ambulatory setting and includes assessment for heart failure symptoms and signs, typical clinical demographics (obesity, hypertension, diabetes mellitus, elderly, atrial fibrillation), and diagnostic laboratory tests, electrocardiogram, and echocardiography. In the absence of overt non‐cardiac causes of breathlessness, HFpEF can be suspected if there is a normal left ventricular (LV) ejection fraction, no significant heart valve disease or cardiac ischaemia, and at least one typical risk factor. Elevated natriuretic peptides support, but normal levels do not exclude a diagnosis of HFpEF. The second step (E: Echocardiography and Natriuretic Peptide Score) requires comprehensive echocardiography and is typically performed by a cardiologist. Measures include mitral annular early diastolic velocity (e′), LV filling pressure estimated using E/e′, left atrial volume index, LV mass index, LV relative wall thickness, tricuspid regurgitation velocity, LV global longitudinal systolic strain, and serum natriuretic peptide levels. Major (2 points) and Minor (1 point) criteria were defined from these measures. A score ≥5 points implies definite HFpEF; ≤1 point makes HFpEF unlikely. An intermediate score (2–4 points) implies diagnostic uncertainty, in which case Step 3 (F1: Functional testing) is recommended with echocardiographic or invasive haemodynamic exercise stress tests. Step 4 (F2: Final aetiology) is recommended to establish a possible specific cause of HFpEF or alternative explanations. Further research is needed for a better classification of HFpEF.

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Pulmonary hypertension (PH) is frequent in left heart disease (LHD), as a consequence of the underlying condition. Significant advances have occurred over the past 5 years since the 5th World Symposium on Pulmonary Hypertension in 2013, leading to a better understanding of PH-LHD, challenges and gaps in evidence. PH in heart failure with preserved ejection fraction represents the most complex situation, as it may be misdiagnosed with group 1 PH. Based on the latest evidence, we propose a new haemodynamic definition for PH due to LHD and a three-step pragmatic approach to differential diagnosis. This includes the identification of a specific “left heart” phenotype and a non-invasive probability of PH-LHD. Invasive confirmation of PH-LHD is based on the accurate measurement of pulmonary arterial wedge pressure and, in patients with high probability, provocative testing to clarify the diagnosis. Finally, recent clinical trials did not demonstrate a benefit in treating PH due to LHD with pulmonary arterial hypertension-approved therapies.

Ghio S, Temporelli PL, Arena R. Tricuspid annular plane systolic excursion and pulmonary arterial systolic pressure relationship in heart failure: an index of right ventricular contractile function and prognosis. Am J Physiol Heart Circ Physiol 305: H1373-H1381, 2013. First published August 30, 2013; doi:10.1152/ajpheart.00157.2013.-Echoderived pulmonary arterial systolic pressure (PASP) and right ventricular (RV) tricuspid annular plane systolic excursion (TAPSE; from the end of diastole to end-systole) are of basic relevance in the clinical follow-up of heart failure (HF) patients, carrying two-to threefold increase in cardiac risk when increased and reduced, respectively. We hypothesized that the relationship between TAPSE (longitudinal RV fiber shortening) and PASP (force generated by the RV) provides an index of in vivo RV length-force relationship, with their ratio better disclosing prognosis. Two hundred ninety-three HF patients with reduced (HFrEF, n ϭ 247) or with preserved left ventricular (LV) ejection fraction (HFpEF, n ϭ 46) underwent echo-Doppler studies and N-terminal pro-brain-type natriuretic peptide assessment and were tracked for adverse events. The median follow-up duration was 20.8 mo. TAPSE vs. PASP relationship showed a downward regression line shift in nonsurvivors who were more frequently presenting with higher PASP and lower TAPSE. HFrEF and HFpEF patients exhibited a similar distribution along the regression line. Given the TAPSE, PASP, and TAPSE-to-PASP ratio (TAPSE/PASP) collinearity, separate Cox regression and Kaplan-Meier analyses were performed: one with TAPSE and PASP as individual measures, and the other combining them in ratio form. Hazard ratios for variables retained in the multivariate regression were as follows: TAPSE/PASP Ͻ/Ն 0.36 mm/mmHg [hazard ratio (HR): 10.4, P Ͻ 0.001]; TAPSE Ͻ/Ն 16 mm (HR: 5

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A hallmark symptom of heart failure (HF) is exercise intolerance, typically evidenced by excessive shortness of breath, and/or fatigue with exertion. In recent years, the physiologic response to progressive exercise using direct measures of ventilation and gas exchange, commonly termed the cardiopulmonary exercise test (CPX), has evolved into an important clinical tool in the management of patients with HF. There is currently debate regarding the optimal CPX response to apply when stratifying risk for mortality, hospitalization, or other outcomes in patients with HF. Early studies in this area focused on the application of peak VO(2) in predicting outcomes in patients considered for transplantation. More recently, the focus of these studies has shifted to an emphasis on ventilatory inefficiency, in lieu of or in combination with peak VO(2), in estimating risk. The most widely studied index of ventilatory inefficiency has been the minute ventilation/carbon dioxide production (VE/VCO(2)) slope. A growing body of studies over the last decade has demonstrated that among patients with HF, the VE/VCO(2) slope more powerfully predicts mortality, hospitalization, or both, than peak VO(2). A number of investigations have also simultaneously examined the diagnostic importance of peak VO(2) and the VE/VCO(2) slope as well as their respective response to various interventions. This review examines the body of evidence which has used aerobic capacity and ventilatory efficiency as prognostic and diagnostic markers as well as endpoints in interventional trials. Based on this evidence, recommendations for future clinical and research applications of these CPX variables are provided.