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WORLD HOSPITAL DIRECTORY
Cardiology Medical European Heart Journal - current issue
<span class="paragraphSection">Cristina Basso specializes in cardiology and pathology and is a professor of pathology at the University of Padua, Italy—home to the world’s oldest anatomical theatre. Her main interests include sudden death, cardiomyopathies and myocarditis, pathology of arrhythmias and conduction tissue, heart tumours, and valve diseases (<span style="font-style:italic;">Figure 1</span>).</span>
<span class="paragraphSection">The Armenian Cardiologists Association (ACA) was established in 1996 by Prof. Karlen Adamyan. Since 1997, the ACA has been a proud member of the European Society of Cardiology (ESC), reflecting its dedication to advancing cardiovascular care and research.</span>
<span class="paragraphSection">The field of cardio-oncology is rapidly gaining momentum, driven by growing clinical and research interest. This progress reflects a heightened awareness of the cardiovascular challenges patients face throughout their cancer journey, including cancer treatment-induced cardiovascular toxicities,<sup><a href="#ehaf052-B1" class="reflinks">1</a></sup> direct cardiac complications of cancer, and the increased cancer risk associated with chronic cardiovascular conditions such as heart failure or ischaemic heart disease.<sup><a href="#ehaf052-B2" class="reflinks">2</a></sup></span>
<span class="paragraphSection">This is a correction to: Christiaan Vrints, Felicita Andreotti, Konstantinos C Koskinas, Xavier Rossello, Marianna Adamo, James Ainslie, Adrian Paul Banning, Andrzej Budaj, Ronny R Buechel, Giovanni Alfonso Chiariello, Alaide Chieffo, Ruxandra Maria Christodorescu, Christi Deaton, Torsten Doenst, Hywel W Jones, Vijay Kunadian, Julinda Mehilli, Milan Milojevic, Jan J Piek, Francesca Pugliese, Andrea Rubboli, Anne Grete Semb, Roxy Senior, Jurrien M ten Berg, Eric Van Belle, Emeline M Van Craenenbroeck, Rafael Vidal-Perez, Simon Winther, ESC Scientific Document Group, 2024 ESC Guidelines for the management of chronic coronary syndromes: Developed by the task force for the management of chronic coronary syndromes of the European Society of Cardiology (ESC) <span style="font-style:italic;">Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS)</span>, <span style="font-style:italic;">European Heart Journal</span>, Volume 45, Issue 36, 21 September 2024, Pages 3415–3537, <a href="https://doi.org/10.1093/eurheartj/ehae177">https://doi.org/10.1093/eurheartj/ehae177</a></span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>The European Union (EU) Medical Device Regulation increased regulatory scrutiny to improve the safety and performance of new medical devices. An equally important goal is providing timely access to innovative devices to benefit patient care. The European Society of Cardiology strongly advocates for the evolution of the Medical Device Regulation system to facilitate priority access for innovative devices for unmet needs and orphan cardiovascular (CV) medical devices in EU countries. Although device approval is currently executed by Notified Bodies in the EU, it will be advantageous in the mid-term to consider a single EU regulatory agency for devices. In the short term, steps can be taken to transform the current system into a more efficient, predictable, cost-effective, and user-friendly service. Key strategies include the following: enhancing predictability of the approval process through use of early scientific advice from regulators; establishing unique regulatory pathways for CV orphan, paediatric, and innovative devices; promoting more efficient (re)certification of essential legacy CV devices; improving transparency of sponsor interactions with Notified Bodies; expanding the roles of the Expert Panels to assist in the approval of CV devices; promoting global regulatory harmonization, considering streamlined authorization of CV medical technologies across selected jurisdictions; developing an efficient system to monitor device safety; and ensuring funding for data collection platforms. Some strategies that could help include considering a pilot programme for joint approval processes of selected devices in partnership with other regions (i.e. US Food and Drug Administration); developing priority pathways for accelerated access to innovative or orphan devices; and increasing recognition of the importance of early feasibility studies in the EU.</span>
<span class="paragraphSection">A 71-year-old male patient with bilateral carpal tunnel syndrome underwent surgical carpal tunnel release procedures. Transthyretin amyloid (ATTR) deposition was revealed in the ligament tissue (<span style="font-style:italic;">Panel A</span>). The patient was referred to our hospital with a symptom of exertional dyspnoea for cardiac investigation. Electrocardiography showed sinus rhythm 73 b.p.m. normal electrical axis, PR duration of 162 ms, and QRS duration of 92 ms, but no low voltage or pseudo-infarct pattern (<span style="font-style:italic;">Panel C</span>). Transthoracic echocardiography indicated no obvious left ventricular (LV) hypertrophy (interventricular septum thickness 11 mm and posterior wall thickness 9 mm), and preserved LV systolic performance (LV ejection fraction = 66%) and diastolic function (<span style="font-style:italic;">E</span>/<span style="font-style:italic;">e</span>′ = 6.9; see Supplementary data onlineSupplementary data online, <span style="font-style:italic;">Video S1</span>, <span style="font-style:italic;">Panel D</span>). Plasma levels of N-terminal pro-brain natriuretic peptide and cardiac troponin T were measured at 11.3 pg/mL (reference value <50 pg/mL) and 0.026 ng/mL (reference value <0.014 ng/mL), respectively. Cardiac magnetic resonance imaging and <sup>99m</sup>Tc-labelled bone scintigraphy showed no evidence of cardiac amyloidosis (see Supplementary data onlineSupplementary data online, <span style="font-style:italic;">Video S2</span>, <span style="font-style:italic;">Panels E</span> and <span style="font-style:italic;">F</span>). Endomyocardial biopsy was performed at the patient’s request. Optical microscopic analysis did not discover amyloid deposits in the endomyocardial biopsy specimen (<span style="font-style:italic;">Panel B</span>); however, amyloid fibrils were revealed by electron microscopy (<span style="font-style:italic;">Panel G</span>). Since no TTR gene mutation was found, the patient was diagnosed with wild-type ATTR amyloidosis.</span>
<span class="paragraphSection">SciLifeLab National COVID-19 Research ProgramKnut and Alice Wallenberg Foundation10.13039/501100004063KAW 2021-0010/VC2021.0018KAW 2020.0299/VC 2022.0008Swedish Research Council10.13039/5011000043592021-050452021-05450Swedish Heart-Lung Foundation10.13039/5011000037932021003020210581ALFGBG-938453ALFGBG-971130ALFGBG-978954Working Life and Welfare10.13039/501100006636FORMAS10.13039/501100001862Research Council for Environment10.13039/501100005876Agricultural Sciences and Spatial Planning2020-02828</span>
<span class="paragraphSection"><strong>This commentary refers to ‘Cardiovascular events following coronavirus disease 2019 vaccination in adults: a nationwide Swedish study’, by Y. Xu <span style="font-style:italic;">et al</span>., <a href="https://doi.org/10.1093/eurheartj/ehae639">https://doi.org/10.1093/eurheartj/ehae639</a> and the discussion piece ‘Clarification on methodology used in the study investigating COVID-19 vaccination and cardiovascular events’, by Y. Xu <span style="font-style:italic;">et al</span>., <a href="https://doi.org/10.1093/eurheartj/ehaf063">https://doi.org/10.1093/eurheartj/ehaf063</a>.</strong></span>
<span class="paragraphSection">A 70-year-old man treated conservatively for type B aortic dissection (<span style="font-style:italic;">Panel A</span>) at the age of 67 was referred to our hospital for surgical repair of aneurysmal dilation of the descending aorta (<span style="font-style:italic;">Panel B</span>). At first, total arch replacement with the frozen elephant trunk technique and surgical aortic valve replacement using an aortic bioprosthesis were performed for ascending aorta dilatation, and moderate aortic regurgitation due to aortic root dilatation (<span style="font-style:italic;">Panel C</span>). Thereafter, two-stage procedures with thoracic endovascular aortic and surgical repair were carried out for chronic post-dissection thoraco-abdominal aneurysm (<span style="font-style:italic;">Panels D, H,</span> and <span style="font-style:italic;">I</span>). Congo red staining of biopsy samples from the descending aorta dissection revealed abundant amyloid deposits (<span style="font-style:italic;">Panels J</span> and <span style="font-style:italic;">K</span>), but not from the aortic valve (<span style="font-style:italic;">Panels E–G</span>). Immunohistochemistry revealed no deposition of transthyretin or immunoglobulin light chain. Laser microdissection-liquid chromatography-tandem mass spectrometry analysis for aortic wall identified amyloidogenic proteins derived from apolipoprotein A-I (ApoA-I). The deposition of ApoA-I related with amyloid protein was confirmed by immunohistochemistry with a specific antibody (<span style="font-style:italic;">Panel L</span>).</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Ambulatory patients presenting with signs or symptoms of heart failure (HF) should undergo natriuretic peptide testing. Rates of death, HF hospitalization, and healthcare costs were examined in patients thus identified with suspected <span style="font-style:italic;">de novo</span> HF.<div class="boxTitle">Methods</div>This population-based study (REVOLUTION HF) encompassing two large healthcare regions in Sweden examined patients who presented to outpatient care for the first time between 1 January 2015 and 31 December 2020, who had a recorded sign (peripheral oedema) or symptom (dyspnoea) of HF, and whose N-terminal pro-B-type natriuretic peptide (NT-proBNP) measured >300 ng/L within ±30 days of that sign or symptom. Characteristics, outcomes, healthcare patterns, and healthcare costs for these patients were followed for 1 year. Comparisons were made with matched controls without history of HF, its signs, its symptoms, or elevated NT-proBNP.<div class="boxTitle">Results</div>Overall, 5942 patients (median age 78.7 years; 54% women) presented with suspected <span style="font-style:italic;">de novo</span> HF. Within 1 year, 29% had received a HF diagnosis. Patients with suspected <span style="font-style:italic;">de novo</span> HF had higher rates of all-cause death (11.7 vs. 6.5 events/100 person-years) and HF hospitalizations (12.5 vs. 2.2 events/100 person-years) than matched controls (<span style="font-style:italic;">n</span> = 2048), with the highest event rates in the weeks after presentation. Rates were higher with higher NT-proBNP levels. Although some patients already used HF guideline-directed medical therapies for other indications, initiation of new medications was variable. Healthcare costs were higher in patients with suspected <span style="font-style:italic;">de novo</span> HF than in matched controls, driven mostly by HF and chronic kidney disease.<div class="boxTitle">Conclusions</div>Patients with suspected HF and elevated NT-proBNP had high mortality and morbidity in the weeks after presentation, and accrued substantial healthcare costs, highlighting an urgent need for prompt identification, evaluation, and treatment of HF.</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Sodium-glucose cotransporter 2 inhibitors (SGLT2i) impact iron metabolism in patients with heart failure but mechanisms are incompletely understood. This <span style="font-style:italic;">post hoc</span> analysis explored interrelations between iron homeostasis, cardiac structure/function, exercise capacity, haematopoiesis, and sympathetic activity at baseline, and the effects of 6-month treatment with empagliflozin vs. placebo by anaemia status in EMPATROPISM-FE study participants.<div class="boxTitle">Methods</div>Myocardial iron content (MIC, estimated by cardiac magnetic resonance T2* imaging), left ventricular (LV) volumes and LV ejection fraction (LVEF), exercise capacity, laboratory iron markers (LIM), haemoglobin/haematocrit, erythropoietin, and plasma norepinephrine were determined at baseline and 6 months.<div class="boxTitle">Results</div>At baseline, 24/80 participants (30%) had anaemia (haemoglobin < 13/<12 mg/dL in men/women). Patients with vs. without anaemia had higher T2* (indicating lower MIC, <span style="font-style:italic;">P</span> < .001), lower peak oxygen consumption (VO<sub>2max</sub>, <span style="font-style:italic;">P</span> = .024) and hepcidin (<span style="font-style:italic;">P</span> = .017), and higher erythropoietin (<span style="font-style:italic;">P</span> = .040) and norepinephrine (<span style="font-style:italic;">P</span> = .016). Across subgroups, lower MIC correlated with higher LV volumes (<span style="font-style:italic;">P</span> < .01) and norepinephrine (<span style="font-style:italic;">P</span> < .001), and lower LVEF (<span style="font-style:italic;">P</span> < .01), VO<sub>2max</sub> (<span style="font-style:italic;">P</span> < .001) and haemoglobin/haematocrit (<span style="font-style:italic;">P</span> < .001). Associations with LIM were poor (all <span style="font-style:italic;">P</span> > .10). Empagliflozin increased MIC (<span style="font-style:italic;">P</span> < .012), improved exercise capacity, and activated haematopoiesis. Changes in LIM and norepinephrine suggested progressive systemic iron depletion and sympatholysis. LV reverse remodelling was greater in individuals with anaemia.<div class="boxTitle">Conclusions</div>Dysregulated cellular iron uptake/availability may be a shared mechanism in myocardial structural/functional impairment, reduced exercise capacity, and restricted haematopoiesis in heart failure, which are worse in patients with anaemia, and improve with empagliflozin. Empagliflozin increases MIC and decreases norepinephrine. Given this inverse association, sympatholysis may help explain the diverse cardiac and systemic benefits from SGLT2i therapy.<div class="boxTitle">Clinical Trial Registration</div>NCT03485222 (<a href="https://www.clinicaltrials.gov">www.clinicaltrials.gov</a>).</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Recurrent myocardial infarction (MI) and incident heart failure (HF) are major post-MI complications. Herein, contemporary post-MI risks for recurrent MI and HF are described.<div class="boxTitle">Methods</div>A total of 6804 patients with a primary discharge diagnosis of MI at 28 Baylor Scott & White Health hospitals (January 2015 to December 2021) were studied. Patient characteristics, treatment, and outcomes, including incident HF, recurrent MI, all-cause death, and all-cause and cardiovascular rehospitalizations, were assessed. Landmark approach anchored at 3 months post-discharge was used to assess 1-year outcomes.<div class="boxTitle">Results</div>Median age was 69 years, 59.7% were male, and 76.7% had non-ST-elevation MI. Comorbidities included hypertension (89%), dyslipidaemia (87%), Type 2 diabetes (48%), and chronic kidney disease (34%); 17% had a history of MI and 23% of HF; 63% underwent percutaneous/surgical revascularization. In landmark-anchored 1-year outcomes (<span style="font-style:italic;">N</span> = 6210), 413 (6.7%) patients died, 1730 (27.9%) had all-cause and 735 (11.8%) cardiovascular hospitalizations, 234 (3.8%) had recurrent MI. Of patients without history of HF, 1160 (23.8%) developed incident HF [42.2%, 26.7%, and 31.1% with ejection fraction (EF) < 40%, 41–49%, and >50%, respectively) within 3 months of discharge. Patients who developed HF had higher risk of death and hospitalizations (all <span style="font-style:italic;">P</span> < .001), irrespective of EF. Of 2179 patients with EF > 50% without prevalent HF or HF during index hospitalization, 257 (11.8%) developed HF and 77 (3.5%) recurrent MI within 1 year.<div class="boxTitle">Conclusions</div>In a contemporary post-MI cohort, the risk for incident HF was greater than recurrent MI, even among those with normal EF and no HF at discharge.</span>
<span class="paragraphSection"><strong>This comment refers to ‘Tirzepatide for Heart Failure with Preserved Ejection Fraction and Obesity’ presented at the American Heart Association’s Scientific Sessions in November 2024 and simultaneously published in the <span style="font-style:italic;">New England Journal of Medicine</span>; <a href="https://doi.org/10.1056/NEJMoa2410027">https://doi.org/10.1056/NEJMoa2410027</a>.</strong></span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>Cardiogenic shock represents a critical condition in which the heart is unable to maintain adequate circulation leading to insufficient tissue perfusion and end-organ failure. Temporary mechanical circulatory support offers the potential to stabilize patients, provide a bridge-to-recovery, provide a bridge-to-decision, or facilitate definitive heart replacement therapies. Although randomized controlled trials have been performed in infarct-related cardiogenic shock and refractory cardiac arrest, the optimal timing, appropriate patient selection, and optimal implementation of these devices remain complex and predominantly based on observational data and expert consensus, especially in non-ischaemic shock. This review explores the details of ‘when, how, and for whom’ temporary mechanical circulatory support devices should be used, examining specific clinical scenarios, the mechanisms by which they operate, and the patient populations that may benefit. The review also highlights the many gaps in evidence and need for better understanding of the interaction between human biology and these devices.</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Current estimates for the lifetime risk to develop heart failure with either a reduced (HFrEF) or preserved ejection fraction (HFpEF) and their associated risk factors are derived from two studies from the USA. The sex-specific lifetime risk and population attributable fraction of potentially modifiable risk factors for incident HFpEF and HFrEF are described in a large European community-based cohort with 25 years of follow-up.<div class="boxTitle">Methods</div>A total of 8558 participants from the PREVEND cohort were studied at baseline from 1997 onwards and followed until 2022 for cases of new-onset HFrEF (ejection fraction < 50%) and HFpEF (ejection fraction ≥ 50%) by assessment of hospital records.<div class="boxTitle">Results</div>A total of 804 cases of new-onset HF were identified (534 HFrEF and 270 HFpEF) during 25 years of follow-up. The mean age at baseline was 50 years for men and 47 years for women. The mean age at onset of HF was 72.1 years in men and 74.2 years in women. The overall lifetime risk of developing HF was 24.5% in men compared to 23.3% in women. The lifetime risk of HFrEF was lower in women compared with men (11.9% vs. 18.1%), while the lifetime risk of HFpEF was higher in women compared with men (11.5% vs. 6.4%). In women, 71% of incident HFrEF cases were attributable to eight risk factors (hypertension, hypercholesterolaemia, obesity, smoking, atrial fibrillation, chronic kidney disease, myocardial infarction, and diabetes mellitus) and 60% in men. In women, 64% of incident HFpEF cases were attributable to those risk factors, whereas this was 46% in men. More specifically, in both men and women, hypertension and hypercholesterolaemia were the strongest risk factors for HFrEF, whereas hypertension and obesity were the strongest risk factors for HFpEF.<div class="boxTitle">Conclusions</div>In this European cohort, the lifetime risk of developing HFrEF was greater in men than in women, while women were at greater risk of developing HFpEF. Eight directly and indirectly modifiable risk factors substantially accounted for the risk of developing HFrEF and HFpEF, particularly in women.</span>
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