The introduction of transcatheter aortic valve replacement (TAVR) has revolutionized the management of aortic stenosis (AS), leading to significant improvements in patient outcomes. Over time, advancements in device technology have further optimized safety and performance of TAVR. However, as the pool of low-risk patients undergoing TAVR expands, many of whom present with concomitant coronary artery disease (CAD), new challenges have emerged. A large proportion of TAVR candidates suffer from CAD, and the clinical implications of this comorbidity remain a subject of debate. Research on the relationship between AS and CAD has yielded conflicting results, but severe CAD is generally linked to worse outcomes in AS patients. The coexistence of AS and CAD complicates diagnosis and management, requiring a comprehensive understanding of both invasive and non-invasive diagnostic techniques, along with careful revascularization strategies. This review explores the prevalence, clinical impact, and diagnostic challenges of CAD in TAVR patients, highlighting emerging methods for its assessment. Key aspects of treatment, including the timing of coronary revascularization, coronary re-access after TAVR in different settings, as well as practical tips and tricks for coronary cannulation, are also discussed. The complexity of managing AS and CAD is further intensified by the need for individualized approaches, particularly in hybrid procedures and subsequent TAVR interventions. Ongoing research and technological innovations offer promising solutions for refining the management of CAD in AS patients undergoing TAVR, with an emphasis on improving prognostic accuracy, optimizing revascularization strategies, and enhancing post-procedural care.

Background: A knee injury in an athlete leads to periods of forced exercise interruption. Myocardial work (MW) assessed by echocardiographic and cardiopulmonary exercise testing (CPET) are two essential methods for evaluating athletes during the period following injury. However, compared to pre-surgery evaluations, the variations in cardiovascular parameters and functional capacity assessed by these methods after surgery remain unclear. Methods: We evaluated 22 non-professional athletes aged 18–52, involved in prevalently aerobic or alternate aerobic/anaerobic sports activities, who were affected by a knee pathology requiring surgical treatment. The evaluation was performed at rest using transthoracic echocardiography, including MW assessment, and during exercise using CPET. Each athlete underwent the following two evaluations: the first before surgery and the second after surgery (specifically at the end of the deconditioning period). Results: Resting heart rate (HR) increased significantly (from 63.3 ± 10.85 to 71.2 ± 12.52 beats per minute, p = 0.041), while resting diastolic and systolic blood pressure, forced vital capacity, and forced expiratory volume in the first second did not show significant changes. Regarding the echocardiographic data, global longitudinal strain decreased from −18.9 ± 1.8 to −19.3 ± 1.75; however, this reduction was not statistically significant (p = 0.161). However, the global work efficiency (GWE) increased significantly (from 93.0% ± 2.9 to 94.8% ± 2.6, p = 0.006) and global wasted work (GWW) reduced significantly (from 141.4 ± 74.07 to 98.0 ± 50.9, p = 0.007). Additionally, the patients were able to perform maximal CPET at both pre- and post-surgery evaluations, as demonstrated by the peak respiratory exchange ratio and HR. However, the improved myocardial contractility (increased GWE and decreased GWW) observed at rest did not translate into significant changes in exercise parameters, such as peak oxygen consumption and the mean ventilation/carbon dioxide slope. Conclusions: After surgery, the athletes were more deconditioned (as indicated by a higher resting HR) but exhibited better resting myocardial contractility (increased GWE and reduced GWW). Interestingly, no significant changes in exercise capacity parameters, as evaluated by CPET, were found after surgery, suggesting that the improved myocardial contractility was offset by a greater degree of muscular deconditioning.

Coronary artery disease (CAD) remains a leading cause of morbidity and mortality worldwide, accounting for over 9 million deaths annually. The prevalence of CAD continues to rise, driven by ageing and the increasing prevalence of risk factors such as hypertension, diabetes, and obesity. Current clinical guidelines emphasize the importance of functional tests in the diagnostic pathway, particularly for assessing the presence and severity of ischemia. While recommended tests are valuable, they may not fully capture the complex physiological responses to exercise or provide the necessary detail to tailor personalized treatment plans. Cardiopulmonary exercise testing (CPET) offers a comprehensive assessment of the cardiovascular, pulmonary, and muscular systems under stress, potentially addressing these gaps and providing a more precise understanding of CAD, particularly in settings where traditional diagnostics may be insufficient. By enabling more personalized and precise treatment strategies, CPET could play a central role in the future of CAD management. This narrative review examines the current evidence supporting the use of CPET in CAD diagnosis and management and explores the potential for integrating CPET into existing clinical guidelines, considering its diagnostic and prognostic capabilities, cost-effectiveness, and the challenges associated with its adoption.

Case report: a 81 years old man with systemic hypertension, dyslipidemia, past smoking habit, was admitted to the ER of our hospital with acute decompensated heart failure. Since July he complained of worsening of dyspnea and paroxysmal nocturnal dyspnea. His blood pressure was of 155/80 mmHg, the HR was of 78 bpm in atrial fibrillation. He reported past myocardial infarction at the age of 32, thenceforth he underwent periodic cardiac check–up. From 2013 he had developed atrial fibrillation. He had suspended Amiodarone because of dysthyroidism, rate control was obtained with Bisoprolol. In 2015, he underwent coronary angiography for a positive scintigraphy showed absence of lesions. During the same hospitalization there was evidence of nocturnal bradycardia (35 bpm). In 2016, a cardiac MR showed subendocardial and intramyocardial fibrosis at mid–basal wall resembling post ischemic events. He underwent past carpal tunnel syndrome surgery. During the actual hospitalization, the EKG showed atrial fibrillation (78 bpm), complete left bundle branch block (both already known). Serum and urinary light–chain assessment and determination of immunoglobulin light chains levels were negative for AL amyloidosis. The echocardiogram documented: hypertrophy of the interventricular septum, mildly reduced LV systolic function (EF=43%). Invasive coronary angiography showed absence of lesions. CMR showed: left ventricular size at the upper limit of normal with hypertrophy of the interventricular septum and the anterior wall, diffused left transmural LGE, focal fibroadipose infiltration of lower basal SIV. During the hospitalization multiple episodes of non sustained ventricular tachycardia occurred, so that a CRT–D device was implanted in secondary prevention. There was a strong suspicion of cardiac amyloidosis so that definitive diagnosis was obtained by the use of 99m Tc scintigraphy coupled with haematologic tests (already done, resulted negative). Scintigraphy showed myocardial uptake of the radiotracer greater than the bone (Grade 3 Perugini score).

Case presentation: A 89-year-old man, with an history of paroxysmal atrial fibrillation and chronic renal disease, was admitted to our ER for acute decompensated heart failure. He reported dyspnea on minimal exertion and worsening peripheral edema. He had a history of heart failure and a severe aortic stenosis first diagnosed in 2020 with an echocardiogram demonstrating a left ventricular ejection fraction (LVEF) of 30% and a low-flow low-gradient aortic stenosis (AVA=0,6 cmq, mean pressure gradient=21 mmHg). Besides, in 2019, he underwent a 99m Tc MDP scintigraphy for a prostatic nodule which showed important myocardial uptake of the bone tracer highly suggestive of cardiac amyloidosis. Urinary light chain assessment and determination of immunoglobulin light chain levels were negative for AL amyloidosis. The electrocardiogram showed: sinus rhythm, low voltage in the frontal leads and complete left bundle branch block with secondary repolarization abnormalities. The patient underwent transthoracic echocardiography for staging the severity of the aortic valve stenosis, which revealed borderline results: the aortic valve area was 0.5 cmq with a transaortic mean pressure gradient of 20 mmHg (EF 25%, with GLS of −5%). Low-dose dobutamine stress echocardiography was performed. At rest conditions, there was global hypokinesia with an ejection fraction of 24%. Aortic valve mean pressure was 19 mmHg referring to a calculated aortic valve opening area of 0,78 cmq. Under peak dobutamine stress (30 mcg/kg/min), LVEF increased to 36%. On the basis of these diagnostic findings, aortic stenosis was classified as pseudo-severe due to systolic dysfunction of the left ventricle with preserved contractile reserve. Besides, aortic calcium score of 574 confirmed that the aortic stenosis was non severe.

A 62–year–old woman, with a history of systemic hypertension, smoking habit and paroxysmal atrial fibrillation treated with Flecainide, was admitted to the ER of our Hospital for chest pain. She reported that the symptoms appeared after an emotional stress at work. Troponin I was of 895 pg/mL. The electrocardiogram showed: negative T waves in the inferior leads and an early repolarization pattern/ ST elevated in the antero–lateral leads. The patient underwent transthoracic echocardiography which showed: EF 45%, akinesia of the posterior and inferior segments of the septum. Invasive coronary angiography showed absence of lesions. CMR presented: EF 51% and mild hypokinesia of the mid septum and inferior segment; signs of oedema affecting the left ventricular myocardium in the apex, the mid inferior segment and in the lower apical wall, with subendocardial hypoperfusion layer in the mid inferior septum (microvascular dysfunction?). The patient was dismissed with the diagnosis of M.I.N.O.C.A. A month later, she was admitted again to our ER suffering from a new episode of acute chest pain; she also reported a short episode of atrial fibrillation (documented by an EKG) lasting about 10 minutes occurred the day before. The EKG showed: negative T waves in anterolateral leads. TnI was of 2052,5 pg/ml. The patient underwent a transthoracic echocardiogram which demonstrated: reduced global systolic function (EF 35%), akinesia of the apex, mid–anterior septum and mid– anterior wall. The day after the echo was repeated and it demonstrated a gaining of Vsx EF which was of approximately of 50%. Invasive coronary angiography showed absence of lesions. A methylergometrine test was negative for vasospasm on anterior descending artery. The CMR showed: EF 58%, signs of oedema in the basal and mid anterior wall, mid–anterior septum. LGE intra wall of the apical septum and of the basal part of the anterior wall (coronary spasm? Vasculitis?) Absence of edema. The final diagnosis was of Tako Tsubo.