Introduction Takotsubo syndrome is a clinical syndrome characterized by typical anamnestic features together with typical ECG and echocardiographic findings. Comparing with the available literature not so many cases of takotsubo syndrome after pacemaker implantation can be found. Furthermore, there are only few articles talking about ECG features in these patient. The case we described allows to observe dynamic ECG alterations in a patient with electro-induced ventriculograms Case Description A 90-year-old male was admitted to the emergency room for important fatigue associated with severe bradycardia (25/min). His cardiovascular history was silent, and his past medical history was characterized by high blood pressure, chronic pulmonary obstructive disease and anemia due to iron deficiency. The ECG showed second degree AVB type 2, with phases of 2:1 AVB and paroxysmal third degree AVB on continuous monitoring. The routine blood tests showed normal T troponin and BNP was 420 pg/mL. The echocardiogram revealed normal biventricular dimensions and systolic function with moderate aortic valve stenosis. The patient underwent urgent permanent DDD pacemaker implantation without previous isoproterenol administration. During the procedure he referred important pain on the site of the wound, and he became confused and agitated. The procedure was complicated by massive pneumothorax that needed quick decompression. On the 2nd day after pacemaker implantation the ECG revealed electro-induced atrium-guided ventriculograms and began to modify with only mild ST-segment elevation in V2 and initial T-wave inversion from V3 to V6 and in I - II - aVF. On the next days, T-waves became deeper and QTc prolonged to 540 ms. These abnormalities were then gradually resolved on the 11th day. Mild transient attenuation of the amplitude of the QRS complexes in V2 – V3 leads on day 1 could be reported. Another echocardiogram was then performed, which showed new apical akinesis with “apical ballooning” aspect and EF of 40%. TnT and BNP values increased. Coronary angiogram was not performed due to patient rejection, so that coronaropathy could not be excluded with certainty. Nevertheless, the patient had only high blood pressure as cardiovascular risk factor and that the probability of the diagnosis of takotsubo cardiomyopathy was assessed of 76,9% by InterTAK diagnostic score, so that we considered Takotsubo syndrome the most likely diagnosis. Therefore, the patient's therapy was then optimized with an increase in the dosage of ACE inhibitors. At one month follow-up the ECG remained stable, and the echocardiogram showed a preserved ejection fraction (EF = 55%), without alterations of the segmental contractility. BNP and TnT values were normal. Therapy was left unmodified. Conclusions Takotsubo syndrome should be consider a rare but possible complication of pacemaker implantation. This is true especially for patients affected by frailty and cognitive impairment. There are no specific ECG criteria for takotsubo syndrome in patients with electro-induced ventriculograms, but anomalies of the repolarization are similar to those in patients with spontaneous ventricular activity. Transient attenuation of the QRS complexes voltages could be seen even just in the precordial leads and it is generally present in the very acute phase.

Hypertrophic cardiomyopathy (HCM) is a common disease, mostly inherited, with a prevalence of 1:500. Cornerstone of the clinical management of HCM patients is stratifying the risk of sudden cardiac death (SCD) which is the most frightening complication despite its relatively low incidence (0,9% per year). Although mathematical risk scores, as proposed by ESC, are the most used to assess the probability of arrhythmic complications leading to SCD, they have been associated with low sensitivity, precluding some high-risk patients from prophylactic ICD implantation. Among the tools at clinicians’ disposal for risk stratification in HCM patients, the latest AHA/ACC guidelines propose an “individual risk markers strategy”, based on the presence of ≥1 clinical feature such as a family history of SCD, extreme left ventricular hypertrophy (LVH), unexplained recent syncope, NSVT, late gadolinium enhancement (LGE) at CMR, systolic dysfunction and LV apical aneurysm. We present a case that lets us reflect on arrhythmic risk stratification. P.C. is a 58 y.o. male with a history of septal hypertrophy (19 mm) and T wave inversion but without an established diagnosis of HCM. He did not have any familiar history of syncope or SCD. He came to the emergency department for epistaxis and was admitted to the cardiology unit due to the previously mentioned findings, where he underwent cardiac-CTA and CMR showing myocardial bridge of left anterior descending artery, LVH with apical aneurysm and LGE areas localized on the apex (transmural) and on the interventricular septum (subendocardial). No signs of dynamic LVOT obstruction or atrial enlargement emerged from echocardiography. During the observation, asymptomatic NSVT were recorded on continuous ECG monitoring. According to the ESC risk prediction score (3.7%) ICD was not strictly indicated but considering the CMR high-risk profile (according to the suggestions of AHA/ACC) we proposed an ICD implantation anyways. The patient refused any invasive procedure and was implanted with a loop recorder. At 12 months remote monitoring showed a single episode of self-terminated sustained polymorphic ventricular tachycardia (02:23 mm: ss) symptomatic of pre-syncope. The patient was then immediately reached and admitted for ICD implantation in secondary prevention. According to the patient's will, and the no need for bradycardia therapy, an S-ICD was implanted. Figure 1LV apical aneurysm at CMRFigure 2Remote Monitoring

No abstract

Propofol infusion syndrome (PRIS) is a rare but potentially lethal side effect of propofol. In most cases it shows various combinations of signs such as unexplained metabolic acidosis, rhabdomyolysis, hepatomegaly, renal failure, hypertriglyceridemia, malignant arrhythmia and rapidly progressive cardiac failure. The development of coved ST elevation in the right precordial leads of the electrocardiogram (ECG), similar to that seen in the type I Brugada syndrome may be the first sign of cardiac instability. There is no specific treatment for PRIS. Successful management consists of an early recognition of its signs followed by a prompt propofol infusion termination. We present the case of a 35-year-old male affected by mild hypertension. He was found by his wife during a transitory loss of consciousness episode. He had resulted positive to Sars Cov 2 infection a day before and was symptomatic for fever and myalgia. An ambulance was immediately called and the patient was transferred to the emergency department for a suspected out-of-hospital-cardiac arrest. The initial one-lead ECG performed by the emergency physician was unremarkable. On arrival he was in a coma state but with stable hemodynamics. ECG showed only an asymmetric T wave inversion in V4-V6 leads. The cardiac echocardiogram did not show any major alterations. In the meantime, due to worsening of respiratory function, orotracheal intubation was performed and the patient was sedated with propofol, midazolam and fentanyl. Subsequently, an episode of atrial fibrillation was documented. Amiodarone infusion was started and the patient reverted to sinus rhythm after a few hours. The following day two episodes of Torsade de Pointes during prolonged QTc (660 ms) occurred. These arrhythmias were treated successfully with magnesium sulfate infusion. Blood analysis showed severe hypokalemia that was immediately corrected. After the hemodynamic stabilization the ECG showed a pattern highly resembling the Brugada pattern type 1 in the right precordial leads. Moreover CPK, myoglobin, high sensitivity troponin I levels started to rise, along with creatinine, triglycerides and markers of hepatic injury. Propofol had been administered continuously for eight days, so PRIS was suspected as the primum movens of this clinical scenario. Propofol infusion was immediately interrupted. Thereafter, the patient gradually improved and was extubated. As soon as the patient's hemodynamic conditions allowed it, a coronary CT and a cardiac MRI were performed, but were unremarkable. To further evaluate the case, a flecainide challenge test was performed, but no significant ECG change was induced. Nonetheless, given both the history of ventricular arrhythmia, the young age of the patient and the unexplained transitory loss of consciousness a subcutaneous defibrillator was implanted as a form of secondary prevention.

Introduction The mechanisms of cardiotoxicity during CAR-T cell therapy remain unclear to this day. We present the case of a 63-year-old woman with diffuse large B-cell lymphoma, who underwent CAR-T cell therapy. Five days after the infusion, she developed takotsubo cardiomyopathy. This is one of the rare cases of CAR-T cell-induced takotsubo cardiomyopathy. Case Description a 63-year-old woman with a diffuse large B-cell lymphoma and without significant cardiovascular history was treated with CAR-T cell therapy. The patient had arterial hypertension, dyslipidemia and history of CAD in the family. Prior to CAR-T cell therapy, she underwent baseline cardiac evaluation with an echocardiogram which showed a normal biventricular function. Within 24 hours of the infusion of CAR-T cells, she developed grade I cytokine release syndrome (CRS) with high-grade fever and sinus tachycardia. On day four, she developed grade three immune effector cell associated neurological syndrome which was treated with tocilizumab and dexamethasone. On day five laboratory testing showed a disproportionate elevation of BNP compared to hs-TnI. An ECG reported diffuse new-onset T wave inversion in all the precordial leads and a prolonged QT interval, and an echocardiogram showed severely reduced left ventricular ejection fraction (EF = 30%) with evidence of apical ballooning and right ventricular systolic dysfunction. Coronary angiography showed significant stenosis of the middle segment of the circumflex artery, which poorly could explain the clinical presentation of the patient. Ventriculography was also performed, which confirmed the ultrasound findings. During the next 48 hours, ECG and left ventricular function improved along with a gradual reduction of BNP and hs-TnI. We concluded that takotsubo syndrome was the most likely diagnosis. The InterTAK score was 89, which corresponded to a probability of takotsubo of 99.4%. The patient's therapy was then optimized with an increase in the dosage of angiotensin receptor antagonists and beta blockers. One month after CAR-T cell infusion, echocardiography showed complete recovery of biventricular function and ECG completely normalized, together with the values of BNP and TnI-hs. Medical treatment was left unmodified. Conclusions the pathophysiology of left ventricular systolic dysfunction during CAR-T cell therapy is unclear, but the main hypotheses are IL-6 mediated myocardial depression during CRS, stress-induced or takotsubo cardiomyopathy, and direct toxicity from CAR-T cells. From the currently available data from retrospective studies, cardiovascular events strongly overlap with CRS and, particularly, with high-grade CRS. Therefore, there is a strong rationale for early treatment with tocilizumab as it has been postulated from retrospective data a lower risk of cardiovascular events with earlier administration of tocilizumab during CRS. Surveillance for cardiotoxicity in patients receiving CAR-T cell therapy is mandatory for prompt recognition and treatment of cardiovascular complications. Our understanding of CAR-T cell-induced cardiomyopathy is still limited, and data regarding predictive factors for persistent cardiac dysfunction are lacking. It is important to differentiate cardiovascular events related to CAR-T cell therapy from epiphenomenon of CRS and capillary leak, to allow for a broader assessment of cardiac events among future CAR T-cell trials.