Severe Left Ventricular Dysfunction Research Articles

Percutaneous Coronary Intervention Versus Optimal Medical Therapy for Severe Ischemic Left Ventricular Systolic Dysfunction

Coronary artery disease is the most common cause of heart failure, which is the leading cause of cardiovascular-related death worldwide. There are insufficient data to make strong recommendations for percutaneous coronary intervention (PCI) in patients with severe ischemic left ventricular systolic dysfunction (LVSD). In that context, we performed a meta-analysis to compare the outcomes of PCI with those of optimal medical therapy alone in patients with severe ischemic LVSD. A systematic search was conducted in PubMed, EMBASE, and ClinicalTrials.gov from inception to December 2023. Our outcome of interest was all-cause mortality in patients undergoing PCI vs medical therapy. We used random effects models to aggregate data and to calculate pooled incidence and relative risk with 95% CIs. Four studies including 2 randomized controlled trials with 2080 patients (PCI, 1082; optimal medical therapy, 998) were included. All-cause mortality did not differ significantly between the groups: 168 patients (15.5%) in the PCI group vs 200 patients (20.0%) in the optimal medical therapy group (relative risk, 0.88; 95% CI, 0.75-1.09; P=.25). In conclusion, the available evidence indicates that PCI does not improve all-cause mortality in patients with severe LVSD without lifestyle-limiting anginal symptoms. Further data are needed to identify subgroups of patients better served by each modality.

Clinical impact of catheter ablation for atrial fibrillation on heart failure parameters

Abstract Background Catheter ablation for atrial fibrillation have already been an established therapy to maintain sinus rhythm in patients with or without heart failure. Atrial fibrillation is often associated with functional valve regurgitations, left ventricular dysfunction and biomarkers of HF. However, it is still unclear how often such parameters improve after catheter ablation. Purpose The aim of this study is to clarify the clinical impact of catheter ablation on heart failure in patients with atrial fibrillation. Methods We retrospectively analysed 139 consecutive patients who underwent catheter ablation for atrial fibrillation and cardiac echocardiography before and one-year after catheter ablation. Patients who underwent hemodialysis or previous valve surgery were excluded. Results Mean age was 69.8±9.5 years and 84(60.4%) patients had persistent atrial fibrillation before ablation procedure. Fourteen (10.1%) patients had severe left ventricular dysfunction (EF<40%). Thirty-four (24.5%) and 37(26.6%) patients had moderate or greater mitral and tricuspid valve regurgitation (MR and TR), respectively. BNP or NTproBNP was significantly elevated in 93(66.9%) patients before catheter ablation. During one-year follow-up, 11 (7.9%) patients underwent second procedure and atrial fibrillation were remained in 2 (1.4%) patients. Additional medications for heart failure were prescribed in 19 (13.7%) of patients after initial procedure. One year after catheter ablation, 19/34(55.9%) and 20/37(54.1%) of moderate or greater functional MR and TR improved to mild or less. Furthermore, 5/14 (35.7%) patients with severe left ventricular dysfunction improved to normal with combined optimal medical treatment. In 64/93 (68.8%) with elevated BNP or NTproBNP, the increase was no longer significant. Even in patients with still elevated BNP or NTproBNP one-year after catheter ablation, their values were decreased by more than 50% in 17/29 (58.6%) patients. Conclusion Catheter ablation for atrial fibrillation can improve heart failure parameters including valve function, systolic ventricular function and biomarkers.

A CATASTROPHIC COMPLICATION OF A CHEST TRAUMA: A CASE REPORT

Abstract A 43 year old patient came to the Emergency Department of our hospital for a cardiology visit. The EKG revealed polymorfic ventricular tachycardia with a heart rate of 160 bpm so that he was admitted to the Intensive Care Unit. In 2005, he had a post traumatic myocardial infarction after a car accident treated with the implantation of one drug eluted stent on the descending artery. Three years later, a single–chamber ICD was placed. On admission in Intensive Care Unit, cardiac auscultation revealed normal heart sounds without murmurs. No lower extremity edema was observed. A transthoracic echocardiogram showed general hypokinesis with reduced global left ventricle systolic function and no pericardial effusion (EF=20%). The patient was haemodynamically stable, the blood pressure was of 130/80 mmHg. The device was also interrogated and it showed six ineffective attempts of antitachycardia pacing. After that, the patient was given an effective intracavitary shock. Moreover, the patient underwent coronary angiography which showed no disease progression and patency of the stent previously implanted on the proximal descending artery. The electrophysiological study was performed and subsequently 3 ventricular ectopic focuses were effectively ablated. Multiple DC shocks were delivered during the procedure and the atrioventricular bundle was damaged. In consideration of the clinical features and the left ventricular reduced ejection fraction, an indication to the implantation of CRT–D was given. Conclusions This case report describes a rare complication of a blunt chest trauma. A young patient with no significant past medical history suffered a dissection of the coronary descending artery resulting in ST–elevation myocardial infarction. The mechanism of coronary occlusion following blunt chest injury may be due to: shear force applied to the coronary arteries leading to intraluminal thrombosis; vascular rupture; embolism to the coronary arteries; fissuring of an atherosclerotic plaque with dislodgment of plaque material; vascular spasm at the site of the injury. Anyway, severe left ventricular dysfunction caused the developing of polymorfic ventricular tachycardia which was unresponsive to medical treatment and was treated with ablation.

DILATED CARDIOMYOPATHY, GUIDELINES PERSONALIZATION OF CARE

Abstract The term Dilated cardiomyopathy (CMD) refers to a family of diseases characterized by complex interactions between environment and genetic predisposition. Diagnostic tools as cardiac magnetic resonance imaging (MRI) must be systematically implemented in clinical practice to define the etiological cause and undertake a specific therapeutic treatment. We present the case of a young man with CMD and severe left ventricular dysfunction (ejection fraction, EF: 14%; left ventricular end–diastolic volume (LVEDV): 251 ml/m2; left ventricular end–systolic volume (LVESV): 197 ml/m2. The patient has a family history of sudden cardiac death (SCD). He is affected by a psychiatric pathology (ADHD) and has a history of alcohol and drug addiction. Many diagnostic hypotheses have been considered for etiological research (viral myocarditis, genetic or alcoholic–induced cardiomyopathy, toxic substances such as narcotics and psychiatric drug–induced cardiomyopathy). MRI after 11 days in hospital confirmed FE 14%, LVEDV: 320 ml/m2, LVESV: 275 ml/m2; reduction of the wall thickness at the antero–septal wall to the middle tract; areas of altered signal, hyperintense in T2W sequences, at the left ventricular myocardial wall suspected of myocardial edema, associated with extended signal hyperintensity of periventricular tissue, which show marked enhancement immediately after intravenous contrast agent administration (Fig. 1). The underlying psychiatric pathology and the possibility of poor adherence to the maintenance of the wearable defibrillator did not facilitate the clinical follow–up which should have included the identification of the etiological cause and the appropriate treatment guaranteeing the temporary prevention of SCD. So, it was decided to make a personalized therapeutic choice, the patient underwent implantation of a subcutaneous defibrillator, pending a better diagnostic definition and the possible need of other therapies as cardiac transplantation/implantation of mechanical assistance device.

YOUNG WOMAN WITH LEFT VENTRICULAR DYSFUNCTION AND MITRAL LAMBL EXCRESCENCE: WHAT TO DO WHEN ISCHEMIC STROKE IS RECURRENT?

Abstract Lambl excrescence describing rare cardiac growths that develop at the valvular coaptation sites of the heart which are seen as a thin, hypermobile and filiform strand on an echocardiogram. These filiform strands can be noted in association with embolic stroke. Also heart failure (HF) and stroke frequently coexist because of an overlap of shared risk factors and subsequent mechanisms and a higher risk of stroke is present also in HF patients in sinus rythm (SR). The clinical case concerns a 54–year–old woman. In March 2020 she was admitted for ischemic stroke by occlusion of middle cerebral artery subjected to thrombolysis and mechanical thromboctomy. Electrocardiogram showed SR and left branch block. Echocardiogram and echocardiogram transesophageal showed left ventricular (LV) dysfunction (EF 40%) withouth clear presence of emboligen sources. Thrombophilic screening and neurological checks were negative. Single antiaggregant therapy has been started. New hospitalization in October 2023 for recurrent ischemic stroke. Echocardiogram showed worsening of LV dysfunction (EF 20%). Transesophageal echocardiogram showed the presence of a filiform filament on the mitral leaflets on the atrial side (Fig 1) without the presence of intracavitary thrombi. Coronary TC angiography (Fig 2) was negative. Cardiac magnetic resonance (Fig 3) confirmed reduced ejection fraction and showed subepicardial late gadolinium enhancement in lateral wall. There are no clear evidence–based guidelines for the treatment of Lambl excrescences. When associated with stroke, an exhaustive stroke workup to identify the potential cause of stroke should always be undertaken. If the workup remains negative without any identifiable cause, then the patients can be treated with antiplatelet agents such as aspirin and clopidogrel or anticoagulation with warfarin. Also the indication to antithrombotic strategies in patients with HF, SR and stroke is controversial. There are no data to support a routine strategy of anticoagulation in patients with HF with LV dysfuncion in SR who do not have history of paroxysmal atrial fibrillation (ESC 2022 HF guidelines). So which therapy to start in young patient, with recurrent strokes, heart failure /severe LV dysfunction and mitral lambl excrescence? Oral anticoagulant? Double platelet antiaggregation? Oral anticoagulant and single platelet antiaggregation? Definitely the choice is not simple but we decided to start warfarin and continue follow–up.

FULMINANT EOSINOPHILIC MYOCARDITIS TREATED WITH STEROIDS AND INTRA–AORTIC BALLOON PUMP

Abstract Background Hypereosinophilic syndrome (HES) is a hematological disorders characterized by a chronic, unexplained hypereosinophilia (HE) with tissue damage. Cardiac involvement occurs in ∼20% of patients with HES and it carries a poor prognosis.Early detection and treatment of myocardial involvement improves prognosis. Immunosuppressive therapy represents the core treatment in the majority of patients with Eosinophilic Myocarditis. Case Summary 50–year–old man with history of intrinsic asthma and HE was admitted for cardiogenic shock B stage according SCAI classification (heart rate was 130 bpm, systolic blood pressure was 90 mmHg and lactate <2). EKG showed sinus tachycardia and diffuse ST segment depression. Echocardiography revealed severe left ventricular systolic dysfunction and mild pericardial effusion. Blood test showed leukocytosis (33x10^9/L) with HE (47%), mild hepato–renal damage, high TroponinT 3874 pg/mL and NT–proBNP 11060 ng/L. Coronary angiography was unremarkable. Pulmonary artery catheter was placed: IC 1,78 l/min/mq, CPO 0,63, WP 21, SVO2 60%, SVR 17 WU, RAP/WP 0.74. We reclassified patients as SCAI C with “mixed shock” due to inflammatory component and latent right ventricular dysfunction. Intra–aortic balloon pump (IABP) was placed and we performed endomyocardial biopsy (EMB). High dose of intra venous corticosteroids was started obtaining progressive improvement of hemodynamic parameters and reduction of inflammation parameters (Fig.1). EMB confirmed the diagnosis of myocarditis with initial transition into ‘’Loffler’s cardiomyopathy’’. Polymerase chain reaction (PCR) analysis did not detect cardiotropic viruses. After improvement of clinical status we performed cardiac MRI that revealed diffuse biventricular myocardial edema and the presence of subepicardial and mid–wall enhancement with non ischemic pattern,endocardial fibrosis and multiple left ventricular thrombi (Fig. 2). β–blockers and angiotensin–converting enzyme inhibitors were started and the patient was discharged at home with a complete myocardial recovery and immunosuppressive therapy based on corticosteroids and azathioprine. Discussion This case demonstrates the usefulness of myocardial biopsy in fulminant myocarditis. Treatment with corticosteroids resulted in rapid improvement. Early invasive monitoring allowed more precise hemodynamic characterization and mechanical circulatory support with IABP proved feasible and might have helped by unloading the left ventricle.

A CASE REPORT OF HEART FAILURE WITH IMPAIRED EJECTION FRACTION DUE TO DILATED CARDIOMYOPATHY IN A YOUNG PATIENT

Abstract A 30–year–old female, with no prior history of heart disease sought medical treatment for increasing shortness of breath, oedema in the lower limbs, abdominal enlargement from seven days. She had was adopted, was a smoker, no use of illicit drugs. Her heart rate was 90 per minute, she had bilateral pitting oedema to mid–shin, her blood pressure was 100/70mm Hg, there were no signs of jugular venous hypertension, the pulmonary and cardiac auscultations were normal. She had ascites and her liver was palpable 3cm below the right costal margin. Her ECG had shown sinus rhythm, heart rate of 92bm, PR interval of 160ms, left bundle branch block (QRS duration of 130ms). Her echocardiogram showed severe global left ventricular dysfunction with left ventricular (LV) ejection fraction (EF) 18% using the apical biplane Simpson’s rule, GLS WAS –4.3%, her right ventricle was dilated and impaired (TAPSE 1,6cm). Her BNP was 2393,90pg/ml. To exclude coronary artery disease, especially congenital coronary artery disease a coronary CT angiography (CTA) was performed. The coronary CTA scan showed normal findings. Cardiac MRI showed severe impairment of both left and right ventricular systolic function with a pattern of gadolinium enhancement negative for necrosis or fibrosis. The patient, after being initially treated with large doses of diuretics and levosimendan, was promptly treated with sacubitril valsartan, empaglifozin, bisoprolol, spironolactone plus vericiguat with rapid titration to maximal tolerated dose. About 1 week later her symptoms began to subside and the patient was discharged in a stable condition. She was referred for consideration of cardiac transplantation and cardiac resynchronisation therapy defibrillator; blood samples for genetic pathology research were taken. A program of serial echocardiograms was introduced, every 30 days, and was observed after 2 months. At follow up our patient had an impressive improvement in terms of improved quality of life, NYHA functional class (from III to I), and performance capacity. A new echocardiographic assessment had shown an LVEF of42% with GLS of–12%. Conclusions: Four pillars of heart failure therapy and vericiguat addiction with rapid titration represents a safe and effective strategy for the treatment of cardiac decompensation with reduced FE. Basal / 60 day EF % 18 /42 GLS % –4.3/ –12.0 E/A 5 /2,1 BNP pg/ml 2393.90 / 889.90 TAPSE cm/s 1.6 / 2.1

DIAGNOSTIC CRITERIA FOR NON–DILATED LEFT VENTRICULAR CARDIOMYOPATHY WITH PROGNOSTIC SIGNIFICANCE

Abstract Background Non–dilated left ventricular cardiomyopathy (NDLVC) is a novel diagnostic entity defined as non–ischemic LV scarring or fatty replacement regardless of the presence of global or regional wall motion abnormalities, or isolated global LV hypokinesia without scarring. While the absence of LV dilation and systolic dysfunction are implicit, no cut–offs were proposed. Methods All patients undergoing cardiac magnetic resonance (CMR) examination at a tertiary referral center from 2012 to 2022 and meeting the definition of NDLVC were evaluated. The primary endpoint was a composite of cardiac death, sustained ventricular tachycardia (VT) or ventricular fibrillation, appropriate defibrillator intervention; the secondary endpoint included also non–sustained VT. Results The cohort included 262 patients, with 176 men (67%) and a median age of 55 years (interquartile range 44–64 years). Patients without moderate (n=243, 93%) or severe LV dilation (n=249, 95%) had a longer survival free from both endpoints. The 50% LVEF threshold identified patients with different outcomes, whereas the 55% and 60% cut–offs did not. LVEF ≥50% and no severe LV dilation predicted a better outcome independent of percent LGE in the LV, the number of LV segments with LGE, LV fibro–fatty replacement, or right ventricular involvement. LVEF ≥50% and no severe LV dilation retained an independent prognostic value even in patients with LV LGE (80% of the whole cohort). Conclusions Excluding severe LV dilation (LVEDVi >129 mL/m2 in men and >116 mL/m2 in women) and LV dysfunction (LVEF <50%) could enhance the prognostic utility of the NDLVC definition.

PARTIALLY REVERSIBLE DILATED CARDIOMYOPATHY ASSOCIATED WITH AMPHOTERICIN B THERAPY

Abstract Background Amphotericin B (AmB) is an antifungal drug commonly used in a broad spectrum of infections, including leishmaniasis. Leishmaniasis, transmitted through insect bites, has cutaneous, mucocutaneous, or visceral (particularly liver and spleen) involvement. The main adverse effects of AmB are cardiotoxicity and nephrotoxicity, often reversible, but with yet unclear pathophysiology. Reversible dilated cardiomyopathy is a rare disease with very few cases described in the literature (less than 10). The Case A 41–year–old man with a silent cardiological history (only cocaine and alcohol abuse in past) is admitted for visceral leishmaniasis. Cardiological evaluation: LBBB in ECG (none previous available); no abnormality detected on ECOCG (EF 55%). Ten days after the AmB cycle, onset of worsening dyspnoea needing hospital treatment after a further two weeks for heart failure (HF). At ECOCG severe left ventricular dysfunction (EF 30%), no rise of cardiac enzymes was detected. Coronary angiography showed 50–75% stenosis on RCA and LAD, treated by angioplasty and stenting. Cardiac MRI showed: dilated left ventricle with diffuse biventricular hypokinesis (FE 16% left and 22% right), areas of LGE of non–ischemic appearance. HFrEF GDMTs were prescribed, with progressive clinical improvement over the next four weeks; at cardiac MRI performed one month later, partially recovery of biventricular function (FE sn 41% right 48%) was found. The ECG showed regression of LBBB. No myocardial biopsy was performed, so it is not possible to get to an unequivocal cardiac dysfunction’s cause. However, the time relationship between the use of AmB and the clinical findings evolution, consistently with the few literature available, suggests a probable diagnosis of AmB toxic cardiomyopathy. An ischaemic cause of the dysfunction is unlikely by the MRI feature and by coronary angiography findings. Literature data suggest that the presence of predisposing factors for cardiac dysfunction, rather than the duration of treatment or preparation used, is the most relevant factor in the development of AmB–related cardiomyopathy. It’s important to perform cardiac monitoring in all patients receiving AmB therapy. In all reported cases, cardiac function recovered substantially after cessation of AmB treatment.

THE INTELLIGENT USE OF ADRENALINE

Abstract Case Report A 52–year–old patient experienced anterior and inferior ST–elevation myocardial infarction, leading to cardiogenic shock necessitating invasive hemodynamic and pharmacological support. During angiography, an intra–aortic balloon pump (IABP) was inserted, and a norepinephrine infusion along with dobutamine was initiated, showing partial clinical and laboratory improvement. Critical disease in all three vessels was detected, prompting angioplasty with stenting of the right coronary artery and left anterior descending artery. Echocardiography revealed severe reduction in left ventricular systolic function (ejection fraction 10%). Despite revascularization and intensive support, the patient‘s hemodynamic status deteriorated (SCAI D), necessitating the addition of adrenaline (0.03 μg/kg/min) to the ongoing dobutamine infusion, suspending noradrenaline. Subsequent days showed gradual improvement, allowing for withdrawal from amine support and discontinuation of the IABP. Follow–up included a cardiac MRI displaying severe systolic dysfunction (EF 21%), extensive ischemic–pattern delayed enhancement across three–vessel distribution. Given the persistent severe left ventricular dysfunction, the patient underwent subcutaneous defibrillator implantation for primary prevention after optimizing anti–remodeling therapy. Despite optimized medical therapy and cycles of levosimendan, the patient experienced heart failure exacerbation, requiring hospitalization (INTERMACS 3). Considering the clinical condition and absence of contraindications, the patient was listed for heart transplantation. Due to refractory hemodynamic instability despite inotropic agents, a left ventricular assist device was implanted as a bridge to transplantation. Roughly 6 months later, the patient successfully underwent heart transplantation without acute complications. Conclusions Very low doses of adrenaline demonstrate increased sensitivity to β2 receptors over α receptors, thereby enhancing mean arterial pressure and peripheral perfusion. At the cardiac level, it induces an increase in both heart rate and coronary blood flow, while peripherally reducing resistances, predominantly due to the prevalence of β2 receptors in skeletal muscle. This improvement contributes to the enhancement of ventricular–arterial coupling. In conditions characterized by a primary pump deficit, such as cardiogenic shock, the use of low–dose adrenaline emerges as a valid therapeutic option.

TAKOTSUBO SYNDROME PRECEDING THE INDEX EVENT: A DANGEROUS CLINICAL SETTING

Abstract We describe the case of a 68–year–old patient who presented to the Emergency Department following an unwitnessed syncopal episode with slow recovery of consciousness. On admission, the patient had dyspnoea together with physical signs of pulmonary congestion. Cardiac ultrasound showed severe left ventricular dysfunction with an ejection fraction of 30%, and apical and paraapical akinesis. The admission electrocardiogram showed sinus tachycardia and diffuse repolarization abnormalities, hs TnI was elevated and BNP vl blood gas analysis were unremarkable. During observation in the Emergency Department, the patient experienced epileptic seizure, promptly resolved by intravenous Midazolam. Contrast–enhanced chest CT ruled out aortic dissection disclosing a clinically irrelevant subsegmental pulmonary embolism. A non–contrast CT scan of the brain yielded negative results. In consideration of the atypical clinical presentation and scattered evidence of an acute coronary syndrome, the patient was admitted to our Cardiac Intensive Care Unit (CICU) for additional diagnostic workup delaying coronary angiography in the presence of stable TnI elevation. Three hours after admission the patient continued showing altered consciousness and a subsequent brain CT was performed, demonstrating an intraparenchymal hemorrhagic spreading. Repeat ECGs showed precordial T wave inversion and prolongation of the QT interval. These data, together with LV apical dysfunction, raised the suspicion of Takotsubo syndrome secondary to an acute cerebrovascular event. During the hospital stay, recovery of consciousness, spontaneous absorption of the cerebral hemorrhagic spread and complete recovery of left ventricular function at repeat cardiac ultrasound examinations were observed, confirming the almost unequivocal diagnosis of Takotsubo syndrome. The patient was discharged uneventfully and was scheduled for an outpatient coronary CT scan. This case underscores the crucial importance of a thorough clinical assessment in the management of complex patients in the presence of nonunivocal clinical signs and misleading blood test and imaging data. Moreover, Takotsubo syndrome is a protean clinical entity that can precede the index event as in our patient, i.e. cerebral hemorrhage. Misclassification of these patients as having an acute coronary syndrome could have led to the initiation of antithrombotic therapy, with potential fatal outcomes for the patient.

THROW YOUR LEAD OVER THE OBSTACLE: A CHALLENGING CRT UPGRADING

Abstract High percentage of right ventricular pacing could lead to pacing induced cardiomyopathy in a non–negligible proportion of patients. Cardiac resynchronization therapy upgrading could represent an option to improve ventricular function, reducing heart failure hospitalizations. A 82 yo male was admitted to hospital with symptomatic heart failure. He had history of complete AV block treated with dual chamber pacemaker implantation five years earlier following coronary artery bypass graft surgery, bioprosthetic aortic valve replacement and septal myectomy. He had also history of cardiac arrest occurred in the context of acute coronary syndrome treated with PCI so that ICD implant was not considered at that time, and two more HF hospitalizations in previous years. Progressive LVEF decline was documented since PM impantation until last echo showed severe left ventricular dysfunction (EF 20% from baseline EF 60%). The ECG showed sinus rhythm and wide paced QRS (206 ms) with 100% pacing percentage. A CRT device upgrading was planned. Baseline venography initially showed pervious axillary–subclavian left axis, but unfortunately the guidewire encountered a complete occlusion before entering the superior vena cava. Nevertheless, dye contrast injection documented the presence of a proximal collateral branch (fig A) having a vertical course in the thorax and reaching the lateral wall of the left ventricle with an extrapericardic course then entering the right heart through inferior vena cava. Using a IM 5Fr sheath (usually used by interventional cardiologists to cannulate internal mammary artery) we could reach this branch, inserting a guidewire and finally advancing a quadripolar lead (Fig B–C) which reached the lateral left ventricular wall. LV capture was confirmed when pacing from the three proximal poles, while the distal one caused phrenic nerve capture. The quadripolar lead was connected to the LV port of a three chamber PM along with previous implanted leads thus obtaining biventricular pacing. QRS paced was 50 ms shorter than baseline. No peri–procedural complications occurred. Lead–related venous occlusion might represent an obstacle to CRT upgrade requiring high technical expertise. The presence of a complete venous occlusion might cause procedural failure, particularly in hospitals without surgical facility. In this case, the presence of a collateral branch reaching the lateral wall of the left ventricle allowed to successfully complete the CRT upgrade.

HEART FAILURE WITH RELAPSING ATRIAL FIBRILLATION: BELOW THE SURFACE

Abstract Advances in pharmacologic and device therapy have greatly improved prognosis of patients with HFrEF. However, the typical clinical course is still characterized by recurring symptoms, worsening functional status and risk of frequent hospitalizations. A 72–years–old male patient with arterial hypertension, poorly controlled T2DM, TIA and chronic kidney disease presented to Cardiology service in 2018 with dyspnoea on effort and first evidence of EF 35% at echocardiography. He was admitted for elective coronary angiography, which demonstrated limited coronary heart disease of circumflex artery and its first marginal branch, treated by PTCA and stenting. CMR confirmed severe LV dysfunction, but also revealed extensive fibrotic areas with ischaemic and non–ischaemic patterns beyond revascularized regions. With such evidences, HF treatments were intensified, with titration of disease– modifying therapies and DOAC was added for asymptomatic paroxysmal AF. CRT–D was implanted for QRS of 160 msec, which was narrowed to 130 msec. Nevertheless, in one–year time the patient presented worsening of symptoms with several hospital admissions for acute HF and AF with fast rate. A switch to rhythm–control strategy was hence chosen. DCCV was performed, after an initial deferral for thrombosis of LAA due to poor adherence to DOAC. However, three–days after DCCV, the patient presented again to emergency services for dyspnoea, left upper flank pain and AF with fast rate. He was admitted to Acute Medicine Unit and treated with high flow O2, iv Furosemide and Digoxin, analgesics. CT chest and abdomen with contrast was performed in the suspicion of systemic venous thromboembolism for persistent type 1 respiratory failure, raised D–dimer and elevated liver function tests, despite appropriate anticoagulation. CT revealed an unexpected left superior pulmonary vein thrombosis, splenic and small left renal infarcts. The patient was discharged after recovery on subcutaneous heparin. At 15–day review, the patient was in stable conditions and awaiting completion of coagulation screening tests. This case study addresses some important aspects in the care of HF. An accurate assessment of HF aetiology and recurrent triggers, a timely planning of pharmacologic and device treatments, alongside with management of co–morbidities, therapeutic adherence and appropriate anticoagulation, can provide the clinician powerful tools to accomplish the difficult task of managing HF below the surface.

Impact of Type 2 Diabetes Mellitus on Left Atrioventricular Coupling and Left Atrial Deformation in Patients with Essential Hypertension: An MRI Feature Tracking Study.

Hypertension (HTN) and type 2 diabetes mellitus (T2DM) are both associated with left ventricular (LV) and left atrial (LA) structural and functional abnormalities; however, the relationship between the left atrium and ventricle in this population is unclear. To identify differences between hypertensive patients with and without T2DM as the basis for further investigation the atrioventricular coupling relationship. Cross-sectional, retrospective study. 89 hypertensive patients without T2DM [HTN (T2DM-)] (age: 58.4 +/- 11.9 years, 48 male), 62 hypertensive patients with T2DM [HTN (T2DM+)] (age: 58.5 +/- 9.1 years, 32 male) and 70 matched controls (age: 55.0 +/- 9.6 years, 37 male). 2D balanced steady-state free precession cine sequence at 3.0 T. LA reservoir, conduit, and booster strain (εs, εe, and εa) and strain rate (SRs, SRe, and SRa), LV radial, circumferential and longitudinal peak strain (PS) and peak systolic strain rate and peak diastolic strain rate (PSSR and PDSR) were derived from LA and LV cine images and compared between groups. Chi-square or Fisher's exact test, one-way analysis of variance, analysis of covariance, Pearson's correlation, multivariable linear regression analysis, and intraclass correlation coefficient. A P value <0.05 was considered significant. Compared with controls, εs, εe, SRe and PS-longitudinal, PDSR-radial, and PDSR-longitudinal were significantly lower in HTN (T2DM-) group, and they were even lower in HTN (T2DM+) group than in both controls and HTN (T2DM-) group. SRs, εa, SRa, as well as PS-radial, PS-circumferential, PSSR-radial, and PSSR-circumferential were significantly lower in HTN (T2DM+) compared with controls. Multivariable regression analyses demonstrated that: T2DM and PS-circumferential and PS-longitudinal (β = -4.026, -0.486, and -0.670, respectively) were significantly associated with εs; T2DM and PDSR-radial and PDSR-circumferential were significantly associated with εe (β = -3.406, -3.352, and -6.290, respectively); T2DM and PDSR-radial were significantly associated with SRe (β = 0.371 and 0.270, respectively); T2DM and PDSR-longitudinal were significantly associated with εa (β = -1.831 and 5.215, respectively); and PDSR-longitudinal was significantly associated with SRa (β = 1.07). In hypertensive patients, there was severer LA dysfunction in those with coexisting T2DM, which may be associated with more severe LV dysfunction and suggests adverse atrioventricular coupling. 3. Stage 3.

Impact of Sex and Diabetes in Patients with Heart Failure.

Heart failure (HF) is a complex clinical syndrome with a growing global health burden. This review explores the intersection of HF, diabetes mellitus, and sex, highlighting epidemiological patterns, pathophysiological mechanisms, and treatment implications. Despite similar HF prevalence in men and women, diabetes mellitus (DM) appears to exert a more pronounced impact on HF outcomes in women. Pathophysiological differences involve cardiovascular risk factors, severe left ventricular dysfunction, and coronary artery disease, as well as hormonal influences and inflammatory markers. Diabetic cardiomyopathy introduces a sex-specific challenge, with women experiencing common adverse outcomes related to increased fibrosis and myocardial remodeling. Treatment strategies, particularly sodium-glucose cotransporter 2 inhibitors, exhibit cardiovascular benefits, but their response may differ in women. The link between HF and DM is bidirectional, with diabetes significantly increasing the risk of HF, and vice versa. Additionally, the impact of diabetes on mortality appears more pronounced in women than in men, leading to a modification of the traditional gender gap observed in HF outcomes. A personalized approach is crucial, and further research to improve outcomes in the complex interplay of HF, diabetes, and sex is needed.

Transcatheter transfemoral aortic valve replacement in a patient with acromegaly and severe left ventricular myocardial hypertrophy. Case report

Main causes of secondary hypertrophic cardiomyopathy include acromegalic cardiomyopathy. Heart damage in patients with the acromegaly is mediated both by the direct action of growth hormone and insulin-like growth factor-1, and increased deposition of collagen and lymphomononuclear cells in the myocardium, which leads to architectural changes, disturbances in fluid and electrolyte balance, severe left ventricular myocardial hypertrophy, diastolic and systolic left ventricular dysfunction and chronic heart failure. This article presents the world's first described observation demonstrating the possibility of successful transfemoral aortic valve repair to a comorbid patient with severe aortic stenosis according to the potential risks caused by the active form of the acromegaly.

Atrial Tachycardia Revealing Obstructive Left Atrial Myxoma. Case Report

Myxomas are the most common primary cardiac tumors; the most common localization is the left atrium, and may cause mitral flow obstruction so their clinical presentation could mimic severe mitral stenosis; trans thoracic echocardiography allows the diagnosis; we report a case of left atrial myxoma revealed by atrial tachycardia concomitant with dyspnea and signs of chronic right heart failure; despite surgical resection of the tumor, our patient had developed tachycardiomyopathy with severe left ventricular dysfunction, which recovered two months later, after intensive administration of antiarrhythmic treatment.

Severe heart failure and intracardiac thrombosis: going beyond the appearance for diagnosis and treatments.

We describe the case of a 45-year-old female affected by asthma and nasal polyposis who presented to the emergency department because of worsening dyspnea and paresthesia of the left lower limb. Comprehensive instrumental examinations revealed the presence of severe left ventricle dysfunction, intra-cardiac thrombus, deep vein thrombosis, pulmonary embolism, lung infiltrates, polyserositis, and neurological involvements. Finally, the patient was diagnosed with eosinophilic granulomatosis with polyangiitis (EGPA), formerly Churg-Strauss syndrome, a rare vasculitis of small-medium blood vessels with several organ involvements. Treatment with anticoagulants, corticosteroids, and cyclophosphamide led to a significant clinical improvement. However, a subcutaneous cardiac defibrillator was implanted because of the persistence of severe left ventricular dysfunction and the high cardiovascular risk phenotype. Indeed, several cardiac manifestations may occur in EGPA, particularly in patients with anti-neutrophil cytoplasmic antibody-negative disease. Therefore, clinicians should have high clinical suspicion because cardiac involvement in EGPA results in a poor prognosis if not diagnosed and adequately treated.

Impact of Anatomical and Viability-guided Completeness of Revascularization on Clinical Outcomes in Ischemic Cardiomyopathy.

Complete revascularization of coronary disease has been linked to improved outcomes in patients with preserved left ventricular (LV) function. To identify the impact of complete revascularization in patients with severe LV dysfunction. Patients enrolled in the REVIVED-BCIS2 trial were eligible if baseline/procedural angiograms and viability studies were available for analysis by independent core laboratories. Anatomical and viability-guided completeness of revascularization were measured by the coronary and myocardial revascularization indices (RIcoro and RImyo) respectively, where RIcoro=[change in BCIS Jeopardy Score (BCIS-JS)] / [baseline BCIS-JS] and RImyo=[number of revascularized viable segments] / [ number of viable segments supplied by diseased vessels]. The PCI group was classified as having complete or incomplete revascularization by median RIcoro and RImyo. The primary outcome was death or hospitalization for heart failure. Of 700 randomized patients, 670 were included. The baseline BCIS-JS and SYNTAX scores were 8 (6 to 10) and 22 (15 to 29) respectively. In those assigned to PCI, median RIcoro and RImyo values were 67% and 85%. Compared to the group assigned to optimal medical therapy alone, there was no difference in the likelihood of the primary outcome in those receiving complete anatomical or viability-guided revascularization (HR 0.90, 95% CI 0.62-1.32 and HR 0.95, 95% CI 0.66-1.35 respectively). A sensitivity analysis by residual SYNTAX score showed no association with outcome. In patients with severe left ventricular dysfunction, neither complete anatomical nor viability-guided revascularization were associated with improved event-free survival compared to incomplete revascularization or treatment with medical therapy alone.

Predictors of Polymorphic Ventricular Tachycardia and Ventricular Fibrillation in Patients with Takotsubo Syndrome

Polymorphic ventricular tachycardia (PVT) and ventricular fibrillation (VF) are life-threatening complications of Takotsubo syndrome (TTS). Data regarding risk factors for PVT/VF based on the TTS variant are lacking. This study aims to identify demographic and clinical factors associated with PVT and VF in patients with TTS. Patients meeting the InterTak criteria for TTS between 2010-2022 were retrospectively identified. The occurrence of PVT/VF with each risk factor was analyzed using logistic regression. Sensitivity analysis was performed to assess the interaction between risk factors. PVT/VF occurred in 27 of the 296 patients with TTS (9.1%). Patients with PVT/VF were younger (52 vs. 62 years, P=0.019) and more frequently used stimulants in the 4 weeks before admission (22.2% vs. 8.2%, OR 3.20, p =0.023). All PVT/VF occurred within 24 hours of hospitalization. An initial QTc threshold of 490 ms had the highest sensitivity and specificity for the occurrence of PVT/VF (AUC=0.687). Patients with PVT/VF were more likely to have a QTc >490 ms on admission (55.6% vs. 18.7%, OR=5.45, P< 0.01), apical variant TTS (78% vs. 56%, OR=2.69, p=0.038), and an admission EF < 30% (63% vs. 41.5%, OR=2.39, p=0.032); each factor was independently associated with PVT/VF irrespective of QTc duration on sensitivity analysis. In conclusion, nearly 1 in 10 of patients with TTS had PVT/VF. A QTc > 490 ms, recent stimulant use, apical variant TTS, and severe left ventricular systolic dysfunction on admission are associated with higher PVT/VF risk, with the first 24 hours being a high-risk period.