Healthcare professional’s guide to cardiopulmonary exercise testing

Cardiopulmonary exercise testing (CPEX) is a valuable clinical tool that has proven indications within the fields of cardiovascular, respiratory and pre-operative medical care. Validated uses include investigation of the underlying mechanism in patients with breathlessness, monitoring functional status in patients with known cardiovascular disease and pre-operative functional state assessment. An understanding of the underlying physiology of exercise, and the perturbations associated with pathological states, is essential for healthcare professionals to provide optimal patient care. Healthcare professionals may find performing CPEX to be daunting, yet this is often due to a lack of local expertise and guidance with testing. We outline the indications for CPEX within the clinical setting, present a typical protocol that is easy to implement, explain the key underlying physiological changes assessed by CPEX, and review the evidence behind its use in routine clinical practice. There is mounting evidence for the use of CPEX clinically, and an ever-growing utilisation of the test within research fields; a sound knowledge of CPEX is essential for healthcare professionals involved in routine patient care

Pneumonitis and pulmonary haemorrhage after acute myocardial infarction

A 55-year-old man presented with acute ST-elevation myocardial infarction. He received rescue angioplasty with one drug eluting stent. He developed marked breathlessness and haemoptysis two days later. Investigations led to the diagnosis of pulmonary haemorrhage, possibly from pneumonitis caused by ticagrelor. He was successfully managed with high-dose steroids and ticagrelor was replaced with clopidogrel. On stopping the steroids a month later, mild haemoptysis recurred and this was managed conservatively. Pneumonitis and pulmonary haemorrhage is rarely reported with acute myocardial infarction, but poses serious challenge to the patient and the clinician. Diagnosis may be delayed as breathlessness can occur due to myriad causes after myocardial infarction. Interrupting dual anti-platelet therapy after angioplasty could lead to devastating stent thrombosis

Cardiopulmonary exercise test in myocardial ischemia detection

Exercise electrocardiography has low sensitivity for detection of myocardial ischemia. However, when combined with cardiopulmonary exercise testing (CPEX), the sensitivity and specificity of ischemia detection improves significantly. CPEX offers unique advantages over imaging techniques in tricky situations such as balanced ischemia. Early abnormal oxygen uptake would point toward profound coronary stenosis that could be missed in perfusion imaging. CPEX could be an invaluable tool in asymptomatic left bundle branch block pattern, without exposing patients to the risks of computerized tomography or invasive coronary angiography. Normal oxygen uptake curves would rule out significant coronary stenosis as the cause of left bundle branch block pattern. Elseways, abnormal oxygen uptake in patients with normal coronary arteries could indicate microvascular angina. Furthermore, exercise capacity is an excellent predictor of cardiovascular risk in those with and without heart disease. Using two clinical cases we introduce the concept of gas-exchange and hemodynamic changes encountered in ischemic heart disease

Smoking status and mortality outcomes following percutaneous coronary intervention

Objective: The aim of this study was to assess the impact of smoking on short (30-day) and intermediate (30-day to 6-month) mortality following percutaneous coronary intervention (PCI). Background: The effect of smoking on mortality post-PCI is lacking in the modern PCI era. Methods: This was a retrospective analysis of prospectively collected data comparing short- and intermediate-term mortality amongst smokers, ex-smokers and non-smokers. Results: The study cohort consisted of 12,656 patients: never-smokers (n = 4288), ex-smokers (n = 4806) and current smokers (n = 3562). The mean age (±standard deviation) was 57 (±11) years in current smokers compared with 67 (±11) in ex-smokers and 67 (±12) in never-smokers; p < 0.0001. PCI was performed for acute coronary syndrome (ACS) in 84.1% of current smokers, 57% of ex-smokers and 62.9% in never-smokers; p < 0.0001. In a logistic regression model, the adjusted odds ratios (95% confidence intervals (CIs)) for 30-day mortality were 1.60 (1.10–2.32) in current smokers and 0.98 (0.70–1.38) in ex-smokers compared with never-smokers. In the Cox proportional hazard model, the adjusted hazard ratios (95% CI) for mortality between 30 days and 6 months were 1.03 (0.65–1.65) in current smokers and 1.19 (0.84–1.67) in ex-smokers compared with never-smokers. Conclusion: This large observational study of non-selected patients demonstrates that ex-smokers and never-smokers are of similar age at first presentation to PCI, and there is no short- or intermediate-term mortality difference between them following PCI. Current smokers undergo PCI at a younger age, more often for ACS, and have higher short-term mortality. These findings underscore the public message on the benefits of smoking cessation and the harmful effects of smoking

Diastolic Ventricular Interaction in Heart Failure With Preserved Ejection Fraction

Background Exercise‐induced pulmonary hypertension is common in heart failure with preserved ejection fraction (HFpEF). We hypothesized that this could result in pericardial constraint and diastolic ventricular interaction in some patients during exercise. Methods and Results Contrast stress echocardiography was performed in 30 HFpEF patients, 17 hypertensive controls, and 17 normotensive controls (healthy). Cardiac volumes, and normalized radius of curvature (NRC) of the interventricular septum at end‐diastole and end‐systole, were measured at rest and peak‐exercise, and compared between the groups. The septum was circular at rest in all 3 groups at end‐diastole. At peak‐exercise, end‐systolic NRC increased to 1.47±0.05 (P<0.001) in HFpEF patients, confirming development of pulmonary hypertension. End‐diastolic NRC also increased to 1.54±0.07 (P<0.001) in HFpEF patients, indicating septal flattening, and this correlated significantly with end‐systolic NRC (ρ=0.51, P=0.007). In hypertensive controls and healthy controls, peak‐exercise end‐systolic NRC increased, but this was significantly less than observed in HFpEF patients (HFpEF, P=0.02 versus hypertensive controls; P<0.001 versus healthy). There were also small, non‐significant increases in end‐diastolic NRC in both groups (hypertensive controls, +0.17±0.05, P=0.38; healthy, +0.06±0.03, P=0.93). In HFpEF patients, peak‐exercise end‐diastolic NRC also negatively correlated (r=−0.40, P<0.05) with the change in left ventricular end‐diastolic volume with exercise (ie, the Frank‐Starling mechanism), and a trend was noted towards a negative correlation with change in stroke volume (r=−0.36, P=0.08). Conclusions Exercise pulmonary hypertension causes substantial diastolic ventricular interaction on exercise in some patients with HFpEF, and this restriction to left ventricular filling by the right ventricle exacerbates the pre‐existing impaired Frank‐Starling response in these patients