bluuebunny/crossref_metadata_2025_split huggingface dataset:
P146 A CASE OF TYROSINE–KINASE INHIBITOR INDUCED CARDIOTOXICITY
Authors: Bellin A , Cutolo A , Antonucci A , Zucca A , Cavalli G , Themistoclakis S 
Published: May 2022

Abstract
This case is about a 69 years–old woman with no prior cardiovascular disease and a history of rheumatoid arthritis;in 2017 underwent right nephrectomy for renal cancer. A few weeks before admission, due to evidence of secondary bone lesions at a follow–up CT–scan, a single dose of the tyrosine kinase inhibitor (TKI) Nivolumab was administered. On the same evening she suffered from a severe reacutization of arthritic symptoms, that led her Oncologist to suspend treatment with nivolumab, and oral corticosteroid therapy was initiated. The following weeks remained though characterized by intense persistent asthenia, severe arthralgias, profuse diarrhea and a syncopal episode; no chest pain was reported. Given the persistence of symptoms, she went to the Emergency Room. Initial work–up revealed a complete heart block, with a previously unknown right bundle branch block (see Figure 1). At blood tests there was a significant increase of troponin I to 7616 ng/L (Normal&lt;12ng/L), BNP 1113 pg/mL (NR &lt; 100 pg/mL), creatinine 2.34 mg/dL (NR 0.55–1.02mg/dL), CPK 1681 U/L (NR 10–145 U/L) and D–dimer 17780 mcg/L (NR &lt; 600). She was immediately transferred to our Cardiologic Intensive Care Unit, where an echocardiogram showed normally functioning ventricular chambers and no valvulopathies. Due to the ongoing acute kidney injury and the history of right nephrectomy, a coronary angiography was not immediately performed, considering the low probability of ACS (no typical symptoms, no regional wall motion abnormalities).Suspecting nivolumab–induced myocarditis, high–dose glucocorticoids were initiated. After a few days we observed persistence of bradycardia and complete AV block despite isoprenaline infusion, and due to signs of peripheral malperfusion (acute kidney injury, hypotension) a definitive leadless pace–maker Micra was implanted (this choice given the need of immunosuppressive therapy that could predispose her to device infections). After normalization of renal function, we performed a coronary angiography that showed normal coronary arteries. Despite the initial improvement of the clinical conditions, the patient suffered a fatal cardiac arrest due to electromechanical dissociation 3 weeks after admission. This case report is an important example showing the significant mortality of cardiotoxicity induced by tyrosine–kinase inhibitors, a side effect that every Cardiologist must be aware of in order to recognize it and immediately intervene with the appropriate therapy.
P148 CANCER INCIDENCE AND MORTALITY ACCORDING TO PRE–EXISTING HEART FAILURE IN A COMMUNITY–BASED COHORT
Authors: Bertero E , Robusto F , Rulli E , D‘Ettore A , Staszewsky L , Maack C , Lepore V , Latini R , Ameri P 
Published: May 2022

Abstract

Background
Studies assessing whether heart failure (HF) is associated with an excess risk of cancer and cancer–related mortality yielded conflicting results. Here, we assessed the incidence and mortality of cancer according to the presence of HF in a community–based cohort.

Methods
By reviewing the health care records of the Puglia region in Italy, we first selected the individuals ≥50–year–old, with no history of cancer within 3 years before the baseline evaluation and ≥5 years of follow–up, during the period from January 1st, 2005 to December 31st, 2013. Next, we matched 1:1 104,020 subjects with HF at baseline and 104,020 controls based on age, sex, Drug–Derived Complexity Index, and follow–up duration. Cancer incidence and mortality were analyzed by Kaplan–Meier method and Cox regression models. Fine and Grey’s regression model was also used to compare cancer–specific mortality while taking into account the competing risk of non–cancer death.

Results
Overall, the mean age of the study population was 76±10 years and the mean follow–up was 5.7 years. The incidence rate of cancer in HF patients and controls was 21.36 (95%CI, 20.98–21.74) and 12.42 (95%CI, 12.14–12.72) per 1000 person/years, respectively, corresponding to a 76% higher risk of incident cancer in HF patients (HR, 1.76; 95%CI, 1.71–1.81). HF patients also died from cancer more frequently than controls (HR 4.11; 95%CI, 3.86–4.38; Figure 1). This excess mortality was highest when age was &lt;70 years (HR 7.54, 95%CI 6.33–8.98), and declined in subjects aged 70–79 years (HR 3.80, 95%CI 3.44–4.19) and ≥80 years (HR 3.10, 95%CI 2.81–3.43). The association of HF with cancer mortality was confirmed in the competing risk analysis (subdistribution HR 3.48, 95%CI 3.27–3.72), as well as the interaction with age: &lt;70 years of age: SHR 6.65, 95%CI 5.60–7.94; 70–80 years: SHR 3.14, 95%CI 2.84–3.48; and ≥80 years: SHR 2.81, 95%CI 2.55–3.10. The HF–related risk applied to the majority of cancer types. Interestingly, among HF patients a high consumption of loop diuretic (≥80 mg/d of furosemide equivalents for ≥30 days in the year before the index date) was associated with a higher mortality for cancer (HR 1.35, 95%CI 1.19–1.53 vs. ≤37.5 mg/d).

Conclusions
The analysis of this large community–based sample suggests that HF does portend an increased risk of cancer and cancer–related mortality, which is blunted, yet remains substantial, with increasing age and competing risk of dying from other causes.
P149 AN UNUSUAL CASE OF CARDIAC TAMPONADE AND ST–SEGMENT ELEVATION MYOCARDIAL INFARCTION
Authors: Bongarzoni A , Tumminello G , Tassinario G , Garagiola M , Carrieri F , Allievi L 
Published: May 2022

Abstract

The case of a 70–year–old woman, a heavy smoker with lung cancer diagnosed in November 2020, is described. The patient underwent 4 cycles of chemotherapy and subsequently a maintenance therapy with atezolizumab. In May 2021, a control CT scan was performed, where multiple cerebral and left adrenal metastases were found. In June 2021, she underwent a cycle of panencephalic radiotherapy. On September 9, 2021, she needed to be admitted to the oncology ward of reference for the appearance, for a few days, of dyspnea due to light exertion and asthenia. In the ward, she was dyspnoic at rest with arterial hypotension (BP 90/60 mmHg). The ECG showed sinus rhythm 110 bpm, anterior STEMI in evolution. The cardiologist performed a bedside echocardiogram which showed abundant pericardial effusion and signs of haemodynamic commitment; akinesia of the apex and middle septum of the left ventricle; LVEF 35%. He was conducted in the angiography room and subjected to pericardiocentesis, guided echo, via the subxiphoid route. 650 ml of blood fluid were removed; on echocardiographic control, a clear reduction of the pericardial effusion was noted. The BP after the procedure went back to 140/80 mmHg and the HR was 100 bpm. Coronary angiography was performed which demonstrated critical stenosis of the mid–segment LAD. After a collegial discussion between the cardiologist and the oncologist which took into account: the presence of haematic pericardial effusion, brain metastatic lesions, a life expectancy &lt;6 months and uncertain date of the heart attack, it was decided not to treat the coronary lesion. A total body CT scan, performed on 13 September, demonstrated widespread and irregular pericardial thickening with nodulations and enhancement due to neoplastic infiltration and the appearance of new metastases in the liver and pancreas. On 14 September, the patient died of respiratory failure. In the literature, only 2 cases are reported with some analogy with the one described.

Conclusion
A rare case of association between haematic pericardial effusion, cardiac tamponade, and myocardial infarction is reported; the priority was to drain the pericardial effusion while the complexity of the case required a collegial assessment between oncologist and cardiologist which led to the decision of not to treat coronary artery lesion on LAD, due to the high risk of bleeding, the short life expectancy and the uncertain date of the heart attack.
P152 R222Q MUTATION OF THE SCN5A GENE IN PEDIATRIC AGE: PHENOTYPE AND RESPONSE TO DRUG THERAPY
Authors: Catucci S , Lombardi M , Vairo U 
Published: May 2022

Abstract

Some studies have shown the association between ventricular and atrial arrhythmias, dilated cardiomyopathy and the R222Q mutation of the SCN5A gene. The mutation causes impaired activation of the sodium channel, the genesis of extrasystoles and the development of dilated cardiomyopathy; both respond better to antiarrhythmic therapy with flecainide and amiodarone than therapy for heart failure. Other studies have shown the efficacy of hydroquinidine.

Purpose of the Study
To observe the clinical characteristics and the response to drug therapy of pediatric subjects carrying the R222Q mutation.

Materials and methods
we observed subjects received at our centre for arrhythmias, carriers of the R222Q variant, subjected to ECG, Echocardiogram, Holter, stress test and follow up.

Results
4 patients were observed, 3 males and 1 female, with ages ranging from 0 to 12 years. The first patient was familiar with dilated cardiomyopathy and rhythm disturbances; he had arrhythmia already in foetal age, he then developed first and second–degree BAV, junctional rhythm and polyform TVNS. Echocardiography and exercise testing were normal. Arrhythmia control was achieved with flecainide. The second patient, with negative familiarity, from the age of 8 is under observation for polyform ventricular ectopic beats, repetitive, unresponsive to propafenone, flecainide, nadolol and sotalol. Echocardiography showed minimal impairment of the contractile function of the left ventricle. Ventricular extrasystoles did not disappear during exertion. At 15, a defibrillator was implanted and hydroquinidine was associated. The third patient presented with foetal tachyarrhythmias; at the age of 6, atrial tachycardia, well–controlled by sotalol, and ventricular ectopic beats were detected. The fourth patient, a cousin of the previous one, developed repetitive ventricular ectopic beats and periods of atrial and junctional rhythm at 12 years; he responded to flecainide.

Conclusions
The R222Q mutation of the SCN5A gene is responsible for arrhythmias already from the pediatric age and is expressed with a variable phenotype. Only one patient with therapy–resistant arrhythmia had contractile dysfunction. Dilated cardiomyopathy could be a consequence of a high arrhythmic burden and occur at a later age if the arrhythmia is not treated. An early and genetic diagnosis is essential.
P174 WELLENS‘ SYNDROME: A TYPICAL CASE
Authors: Dell‘Uomo M , Bier N , Carreras G , Lazzari L , Dominioni I , Nicolì L , Dominici M 
Published: May 2022

Abstract
78–year–old man, hypertensive, diabetic, dyslipidemic, with a recent diagnosis of chronic ischemic encephalopathy and cognitive impairment that severely limited the acquisition of both proximate and remote pathological anamnesis.Transported to the emergency room from 118, contacted by family members, due to pain in the left arm associated with cold sweating and general malaise, symptoms lasting about 4 hours and no longer present upon arrival in the emergency room.On the Echocardiogram performed in ER: akinesia of the apex in its entirety and of the middle anterior wall, not present in a previous examination in April. To laboratory tests: first determination of the high sensitivity troponin within the limits of the norm. On ECG: sinus rhythm at 96 bpm, PR interval 144 ms, left axial deviation, elevation of the ST tract. at J point &lt;1 mm with presence of biphasic T waves in V2–V3. QTc Bazett 409 ms.The patient was then taken to the hemodynamics room and subjected to angioplasty on the proximal anterior descending artery, for critical stenosis of the same. The case is a typical example of Wellens‘ Syndrome.It represents an electrocardiographic manifestation of critical stenosis of the proximal anterior interventricular artery in patients with unstable angina, which is associated with a high risk of developing extensive anterior infarction with a severe prognosis.Originally classified as two separate types, today it is considered as the evolution of type 1 into type 2, manifesting initially with biphasic inversions of the T wave (observed only in 25% of patients with Wellens) and, subsequently, with symmetrical inversions, often deep (&gt; 2 mm) of the T wave, in the anterior precordials.This electrocardiographic aspect is typically present in the absence of pain, while the electrocardiographic trace generally normalizes in presence of pain.After coronary revascularization, most patients show normalization of the electrocardiogram and often of sectoral abnormalities of left ventricular function, suggesting that underlying the electrocardiographic and echocardiographic changes observed in Wellens is a mechanism of myocardial hibernation or stunning.
P182 VALSARTAN LIMITS PULMONARY AND CARDIAC DAMAGE INDUCED BY SARS–COV–2 IN EXPERIMENTAL MODELS BY REDUCING THE EXPRESSION OF ACE2
Authors: Bastaroli F , Mura M , Sammartino J , Ferrari A , Corli M , Guarona C , Percivalle E , Gnecchi M 
Published: May 2022

Abstract

Background
SARS–CoV–2 primarily affects the respiratory system, but cardiac complications also occur very often. The entry of SARS–CoV–2 into host cells is mediated by the interaction between the viral glycoprotein Spike (S) and the host angiotensin–converting enzyme 2 (ACE2) protein. The use of ACE inhibitors (ACEIs) and angiotensin II type 1 receptor blockers (ARBs) might influence both ACE2 expression and viral infection, but our knowledge about these possible interactions is limited. Aim. To evaluate the effects of ACEIs and ARBs during active viraemia.

Methods
We tested the effects of exposure to the ACEI Lisinopril (100nM and 500nM) and the ARB Valsartan (10µM and 50µM) on three different cell types: green monkey–derived epithelial cells (VERO E6) which are used to replicate SARS–CoV–2, cardiomyocytes derived from hiPSC (iPSC–CMs) as heart model and a lung epithelial cancer cell line (16HBE) as pulmonary model. The SARS–CoV–2 wild strain was inoculated on cell lines for 1 hour. Cell viability was measured 72 hours after infection. The supernatants of the infected cells were collected and titrated by the micro–neutralization assay on VERO E6 cells to verify the presence of the virus. Levels of ACE2 mRNA and protein content on cell lysates were quantified after each treatment by RT–qPCR and western blot, respectively.

Results
ACEI and ARB at both concentrations do not affect the viability of the 3 cell lines. Vice versa, viral infection significantly decreases the viability of VERO E6 (–60%, p &lt; 0.0001) and iPSC–CMs (–44%, p &lt; 0.001), while 16HBE cells do not show a cytopathic effect after infection. Viral titration shows that SARS–CoV–2 replicated in cell lines and was actively released into supernatants. Valsartan 50µM decreased virus release in the three cell lines and increased the viability of VERO E6 (+69%, p &lt; 0.01) and iPSC–CMs (+20.5%, p &lt; 0.05) after the infection. Valsartan 50µM also decreases both mRNA (–65% in VERO E6, p &lt; 0.001; –50% in iPSC–CMs, p &lt; 0.05; –60.5% in 16HBE, p &lt; 0.01) and protein levels of ACE2 in all 3 cell lines.

Conclusion
The data suggest that ACEIs and ARBs do not worsen the SARS–CoV–2 infection and that Valsartan, by reducing the levels of ACE2 expression, might result protective.
P185 META–ANALYSIS OF PLACEBO–CONTROLLED TRIALS OF LEVOSIMENDAN IN ACUTE MYOCARDIAL INFARCTION
Authors: Tumminello G , Cereda A , Laricchia A , Carlà M , Conconi B , Barbieri L , Lucreziotti S , Carugo S 
Published: May 2022

Abstract

Introduction
Despite the potential beneficial effects in the acute phase of myocardial infarction, the use of Levosimendan in recent guidelines is currently limited to patients with heart failure and a severe reduction in cardiac output not responding to standard therapy. In spite of everything, the haemodynamic effects of the drug that reduces afterload, the beneficial pleiotropic effects on myocardial stunning and the improvement of microcirculatory indices make Levosimendan still an interesting therapeutic prospect in AMI.

Purpose of the Study
The study aimed to analyse the available data of the use of Levosimendan in the acute setting of myocardial infarction Materials and Methods This review was registered in the International Prospective Register of Systematic Reviews (PROSPERO) and was conducted and presented according to best practice recommendations, including the Preferred Reporting Items for Systematic Reviews and Meta–Analyses (PRISMA) reporting guidelines. Seven selected studies were included in the meta–analysis. Meta–Analysis Levosimendan treatment was associated with a reduction in one year mortality and adverse event rates, without inconsistency. A trend of the increase of cardiac index and reduction of wedge pressure was evident, with an inconsistent effect on blood pressure and heart rate. No evidence of small study effects was found upon the inspection of funnel plots or regression tests. Finally, possibly given the limited number of included studies, metaregression analysis did not identify any major effect modifier.

Discussion
A clearly significant mortality reduction in the acute phase and long–term mortality induced by Levosimendan in AMI is evident. In the acute ischemic field, the haemodynamic properties of Levosimendan may explain part of the benefits. Levosimendan, over an inotropic effect, has a positive effect on ventriculo–arterial coupling, peripheral vasodilation consequently increasing tissue perfusion, anti–stunning effects and anti–inflammatory effects.

Conclusions
Our data support the idea that Levosimendan may already have a role in the treatment of acute ischemic heart disease. Further studies, specifically designed to investigate the early role in the treatment of ischemic heart failure are needed.
P230 CARDIOGENIC SHOCK NETWORK: FROM PRIMARY PERCUTANEOUS CORONARY INTERVENTION TO VENTRICULAR ASSIST DEVICE IMPLANTATION
Authors: Sorini Dini C , Maccherini M , Bernazzali S , Natali B , Codecasa R , Antenore A , Bellandi F , Valente S 
Published: May 2022

Abstract

We report the clinical case of a 75 year–old man, previous smoker with mild lower extremity arterial disease, that presented a sudden and intensive chest pain. The emergency medical system documented an anterior STEMI quickly complicated by out–of–hospital cardiac arrest from a shockable rhythm, treated with DC–shock with rapid ROSC and recovery of consciousness. The patient was transported to the local hospital where coronary angiography showed extensive intraluminal thrombosis of ostial Cx and ostial LAD treated with thrombus aspiration and balloon angioplasty. During the procedure the patient was supported with inotropic agents, mechanical ventilation and IABP for a cardiogenic shock. After few hours he was transferred to level II hospital, equipped with all mechanical circulatory supports (MCS) and on–site cardiac surgery, where he was assisted with vaso–inotropic drugs, Impella CP and continuous renal replacement (CRRT). After 3 days for a refractory cardiogenic shock (stage D) the patient was referred and then transferred to our hospital, a level III hospital with cardiac transplantation program, for hemodynamic stabilization and eventual long term ventricular assist device (VAD). After 5 days the patient was weaned by Impella support, then weaned by mechanical ventilation, renal replacement therapy, without any neurological damage. The echocardiography showed a severe left ventricular dysfunction (EF 20%) with severe mitral regurgitation with good right ventricle function, confirmed also by strain assessment. In the following weeks were reported repeated episodes of pulmonary congestion treated with high doses of diuretics, NIV and nitroprusside infusion and episodes of low cardiac output treated with inotropes for prolonged periods. Mitraclip implantation was technically feasible but Heart Team decided to implantation an LVAD due to numerous episodes of low cardiac output and reduced cardiac index values. Screening for VAD showed no contraindications, therefore after 72 days from acute event LVAD was implanted with positive outcome.

Conclusion
the presence of a local network for cardiogenic shock allowed to optimize the clinical pathway of this patient and to manage in an integrated way the complex treatment of cardiogenic shock.
P263 ROLE OF VITAL SIGNS AND INDICES OF SHOCK DERIVED FROM THEM IN THE SUSPICION OF MASSIVE PULMONARY EMBOLISM IN ELDERLY: THE ER AS A WINDOW ON REAL LIFE
Authors: Savioli G , Brattoli M , Fumoso F , Lapia F , Mugellini A , Martignoni A , Ceresa I , Muzzi A , Novelli V , Preda L , Lava M , Manzoni F , Bressan M 
Published: May 2022

Abstract

Purpose
Assess which vital parameters or shock parameters, in the real life of an Emergency Department, correlate with the presence of massive pulmonary embolism to see which ones can be of help to early suspect it.

Methods
Single–center retrospective observational study, on all geriatric patients (&gt; 75 y) who entered our ED, where they were diagnosed with acute PE. Enrollment began in 2016 and ended in 2019. We collected data from medical history, physical examination, laboratory tests, imaging; we calculated the characteristic scores from the diagnostic / therapeutic algorithm, both for the risk of PE (Wells, Geneva and Anni), and for the presentation of the risk of mortality at 30 days (sPESI). We then had all chest CTs retested by an experienced radiologist. We assess the correlation of vital parameters and shock indexes with the presence of massive pulmonary embolism. We took into consideration: the shock index (SI), the modified shock index (MSI) and the age–shock index (AGE_SI).

Results
We enrolled 247 patients, with a mean age of 83 years and prevalence of female (F = 63%). Of these, 85 (34.4 %) presented with massive pulmonary embolism. There is no correlation between blood pressure, systolic and diastolic values, respiratory rate with the presence of massive pulmonary embolism (p &gt; 0.05). However, there is a strong statistical correlation between heart rate values and the presence of massive pulmonary embolism (p &lt; 0.0001). The shock index correlates with the presence of massive pulmonary embolism with good statistical strength (p &lt; 0.001); the modified shock index correlates with the with even greater statistical strength (P = 0.0005). The age–shock index correlates with the presence of pulmonary embolism with excellent statistical strength (p &lt; 0.0001).

Conclusions
The study suggests that the alteration of shock indices, in particular of the AGE–shock index, correlate with the condition of massive pulmonary embolism. Taking into consideration these parameters, of very low cost, available from triage and obtainable in a few minutes at the medical examination, easily performed in the various Italian situations, can help to raise the suspicion of massive pulmonary embolism early and direct the patient more quickly towards the correct procedure therapeutic diagnostic.