Browsing by Author "Guazzi, Marco (7102760456)"

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. © 2020 European Society of Cardiology

Background Revascularization appears to be beneficial only in patients with high levels of ischemia. This study examined the utility of gas analysis during the recovery phase of cardiopulmonary exercise testing (CPET) in predicting coronary artery disease (CAD) severity and prognosis. Methods 40 Caucasian patients (21.2% females), mean age 63.5 ± 7.6 with significant coronary artery lesions (≥ 50%) were studied. Within two months of coronary angiography, CPET on a treadmill (TM) and recumbent ergometer (RE) were performed on two visits 2–4 days apart; subjects were subsequently followed 32 ± 10 months. Myocardial wall motion was recorded by echocardiography at rest and peak exercise. Ischemia was quantified by the wall motion score index (WMSI). Results Mean ejection fraction was 56.7 ± 9.6%. Patients with 1–2 stenotic coronary arteries (SCA) showed a poorer CPET response during the recovery phase than patients with 3-SCA. ROC analysis revealed the change of carbon-dioxide output (∆ VCO2) recovery/peak (area under ROC curve 0.77, p = 0.02, Sn = 87.5%, Sp = 70.4%) and oxygen uptake (∆ VO2) recovery/peak during TM CPET (area under ROC curve 0.76, p = 0.03, Sn 75.0%, Sp 77.8%) were significant in distinguishing between 1-2-SCA and 3-SCA. The same variables predicted ΔWMSI peak/rest on univariate analysis (p < 0.05). Multivariate Cox analysis revealed a high predictive value of ∆ VO2 recovery/peak obtained during TM CPET for composite endpoint of cumulative cardiac events (HR = 1.27, CI = 1.07–1.51, p = 0.008). Conclusions The current study suggests CPET parameters in recovery hold predictive value for CAD severity and prognosis. TM testing seems to be a better approach in the assessment of CAD severity and prognosis. © 2017 Elsevier B.V.

Aim: We sought the cardiopulmonary exercise testing (CPET) parameter that most accurately reflected therapeutic efficacy in patients with hypertrophic cardiomyopathy (HCM). Methods: Well-being questionnaire, N-terminal brain natriuretic peptide measurements, echocardiography, and CPET were performed in patients with symptomatic non-obstructive HCM during phase II, randomized, open-label multicentre study, before and after 16 weeks of traditional or sacubitril/valsartan treatment. Patients were followed 36 months after the initial CPET. Primary endpoints were changes in: 1) peak oxygen consumption (VO2); 2) VO2 at anaerobic threshold (AT); 3) oxygen pulse; 4) minute ventilation (VE)/carbon-dioxide (CO2) production slope; 5) VE/VCO2 at AT (VE/VCO2_AT); 6) VE/VCO2 nadir; 7) VE/VCO2 intercept; and 8) partial end-tidal pressure of carbon-dioxide (PETCO2) change during CPET. Results: Of 115 screened patients, 61 (52 ± 14 years, 43 % women) were included. Within subject therapy effects were detected only by the VE/VCO2 intercept and PETCO2 change, whereas the differences between medical regimens were detected by differences in VE/VCO2 nadir and VE/VCO2_AT changes after the treatment. The best predictors of the change in well-being were left ventricular outflow tract maximal gradient and VE/VCO2 intercept (B = 0.41,0.36; SE = 0.16,0.30; CI = 0.14–0.79, 0.15–1.14; p = 0.006,0.016, respectively). Adverse cardiac events were best predicted by the initial VE/VCO2 nadir. Conclusion: Ventilatory efficiency parameters outperform peak VO2 in gauging therapy effects in patients with HCM. © 2024 Elsevier Inc.