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WORLD HOSPITAL DIRECTORY
Cardiology Medical European Heart Journal - current issue
<span class="paragraphSection">The global challenge to decrease the burden of cardiovascular disease has led to a critical examination of how we train future cardiologists. As the field evolves, there's a growing recognition that future doctors need comprehensive training to address the complex challenges ahead. However, significant differences persist in cardiology curricula across the Atlantic, reflecting varied approaches to medical education and healthcare systems.</span>
<span class="paragraphSection">Netherlands Organization for Health Research and Development10.13039/501100001826NWO10.13039/501100003246European Research Council10.13039/501100000781ERC-2024-STG-101161004ERC-2014-CoG-648916Netherlands Organization for Health Research and Development</span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Accurate near-term prediction of life-threatening ventricular arrhythmias would enable pre-emptive actions to prevent sudden cardiac arrest/death. A deep learning–enabled single-lead ambulatory electrocardiogram (ECG) may identify an ECG profile of individuals at imminent risk of sustained ventricular tachycardia (VT).<div class="boxTitle">Methods</div>This retrospective study included 247 254, 14 day ambulatory ECG recordings from six countries. The first 24 h were used to identify patients likely to experience sustained VT occurrence (primary outcome) in the subsequent 13 days using a deep learning–based model. The development set consisted of 183 177 recordings. Performance was evaluated using internal (<span style="font-style:italic;">n</span> = 43 580) and external (<span style="font-style:italic;">n</span> = 20 497) validation data sets. Saliency mapping visualized features influencing the model’s risk predictions.<div class="boxTitle">Results</div>Among all recordings, 1104 (.5%) had sustained ventricular arrhythmias. In both the internal and external validation sets, the model achieved an area under the receiver operating characteristic curve of .957 [95% confidence interval (CI) .943–.971] and .948 (95% CI .926–.967). For a specificity fixed at 97.0%, the sensitivity reached 70.6% and 66.1% in the internal and external validation sets, respectively. The model accurately predicted future VT occurrence of recordings with rapid sustained VT (≥180 b.p.m.) in 80.7% and 81.1%, respectively, and 90.0% of VT that degenerated into ventricular fibrillation. Saliency maps suggested the role of premature ventricular complex burden and early depolarization time as predictors for VT.<div class="boxTitle">Conclusions</div>A novel deep learning model utilizing dynamic single-lead ambulatory ECGs accurately identifies patients at near-term risk of ventricular arrhythmias. It also uncovers an early depolarization pattern as a potential determinant of ventricular arrhythmias events.</span>
<span class="paragraphSection">A 53-year-old male presented with intermittent chest tightness for the past month, but denied chest pain or dyspnea during physical exertion. Laboratory tests were unremarkable. Cardiac ultrasound identified a mass in the right atrioventricular groove. Non-contrast cardiac CT revealed a soft tissue mass with heterogeneous density in the same region. Post-contrast, the lesion showed no significant enhancement during the arterial phase (<span style="font-style:italic;">Figure A</span>). Volume rendering demonstrated a well-defined mass encircling the right coronary artery (<span style="font-style:italic;">Figure B</span>, marked by an asterisk), without causing luminal stenosis, and adjacent to the coronary-pulmonary arterial fistula (<span style="font-style:italic;">Figure B</span>, arrow).</span>
<span class="paragraphSection"><strong>This comment refers to ‘De-escalation to ticagrelor monotherapy versus 12 months of dual antiplatelet therapy in patients with and without acute coronary syndromes: a systematic review and individual patient-level meta-analysis of randomised trials’ which was published in The Lancet, <a href="https://doi.org/10.1016/S0140-6736(24)01616-7">https://doi.org/10.1016/S0140-6736(24)01616-7</a>.</strong></span>
<span class="paragraphSection"><strong>This commentary refers to ‘Accelerated atrial pacing reduces left-heart filling pressure: a combined clinical-computational study’, by T. van Loon <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehae718">https://doi.org/10.1093/eurheartj/ehae718</a> and the discussion piece ‘Increasing heart rate in heart failure with preserved ejection fraction: a sensible way to go?’, by P. Sen <span style="font-style:italic;">et al.</span>, <a href="https://doi.org/10.1093/eurheartj/ehaf109">https://doi.org/10.1093/eurheartj/ehaf109</a>.</strong></span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div>Over the past decade, leadless pacing has undergone a rapid evolution, resulting in multiple leadless pacemaker (LPM) devices that offer advancements such as atrioventricular synchronized pacing in VDD mode, atrial stimulation, dual-chamber pacing, and longer battery longevity. Studies comparing LPMs with transvenous pacemakers (TVPMs) show a lower rate of device-related complications with LPMs. In the near future, LPMs could be combined with other devices such as non-transvenous implantable cardioverter-defibrillators to provide anti-tachycardia pacing or bradycardia pacing. Future prospectives for leadless cardiac resynchronization therapy and leadless conduction system pacing are being investigated. As LPMs continue to improve, their applications are anticipated to expand further improving patient outcome, promising a bright future for leadless pacing. In this review, the past, present, and future of leadless pacing are discussed with a focus on cutting-edge implantation techniques, clinical outcomes, and modern advancements of LPMs.</span>
<span class="paragraphSection"><strong>Holger Thiele, Medical Director of Cardiology at the Heart Center Leipzig, Germany—one of Europe’s largest heart centres—is known for groundbreaking multicentre trials that have transformed our understanding and treatment of cardiogenic shock and acute coronary syndromes (<span style="font-style:italic;">Figure 1</span>).</strong></span>
<span class="paragraphSection"><div class="boxTitle">Abstract</div><div class="boxTitle">Background and Aims</div>Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndrome (ACS). Recent data suggest a harmful association of dual antiplatelet therapy compared with single antiplatelet therapy following SCAD. This study investigated independent predictors of major adverse cardiovascular events (MACEs) and recurrence in patients with SCAD.<div class="boxTitle">Methods</div>This multicentre cohort study involving 23 Australian and New Zealand sites included patients aged ≥18 years with an ACS due to SCAD confirmed on core laboratory adjudication. Multivariable Cox proportional hazard models analysed predictors for the primary MACE outcome.<div class="boxTitle">Results</div>Among 586 patients, 505 (150 prospective, 355 retrospective) with SCAD confirmed by core laboratory adjudication, mean age was 52.2 ± 10.6 years, 88.6% were female, and 74.5% were Caucasian. At long-term follow-up (median 21 months), MACE and SCAD recurrence occurred in 8.6% and 3.6% of patients, respectively. Oral anticoagulation on discharge [adjusted hazard ratio (aHR) 3.8, 95% confidence interval (CI) 1.6–9.3, <span style="font-style:italic;">P</span> = .003], ticagrelor combined with aspirin (aHR 1.8, 95% CI 1.04–3.2, <span style="font-style:italic;">P</span> = .037), fibromuscular dysplasia (aHR 2.2, 95% CI 1.05–4.5, <span style="font-style:italic;">P</span> = .037), and history of stroke (aHR 3.8, 95% CI 1.2–12.2, <span style="font-style:italic;">P</span> = .03) were independently associated with higher MACE. Fibromuscular dysplasia (aHR 3.9, 95% CI 1.5–26.5, <span style="font-style:italic;">P</span> = .01), ticagrelor combined with aspirin (aHR 2.6, 95% CI 2.1–5.3, <span style="font-style:italic;">P</span> = .01), and history of stroke (aHR 6.2, 95% CI 1.8–9.5, <span style="font-style:italic;">P</span> = .01) were also associated with higher SCAD recurrence.<div class="boxTitle">Conclusions</div>The findings support the hypothesis that SCAD is primarily caused by intramural bleeding, with a harmful association of more potent antiplatelet therapy and anticoagulation with adverse cardiovascular outcomes.</span>
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