scholarly journals 717 A case of takotsubo cardiomyopathy due to… fear of COVID

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Annita Bava ◽  
Stefano Postorino ◽  
Sebastiano Lanteri ◽  
Francesco Ciancia ◽  
Francesco Antonio Benedetto
Keyword(s):  
Left Ventricle ◽  
Takotsubo Cardiomyopathy ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Hemodynamic Instability ◽  
Left Ventricular ◽  
Mitral Insufficiency ◽  
St Segment Elevation ◽  
St Segment ◽  
As Stress

Abstract Takotsubo syndrome (TTS), also known as ‘stress cardiomyopathy’ or ‘broken heart syndrome’, is a frequent cause of transient ST-segment elevation, characterized by typically reversible abnormalities of segmental kinetics of the left ventricle, triggered by emotional or physical stress, with not critical stenosis at coronarography. This cardiomyopathy mainly affects women (about 90% of cases), especially in the post-menopausal age, and owes its names to the typical shape of the left ventricle in telesystole to ventriculography (‘takotsubo’ is a Japanese term for a vessel used as an octopus trap, with a thin neck and rounded tip). The incidence of Takotsubo cardiomyopathy showed a marked increase during the COVID-19 pandemic. On the other hand, a marked worsening of anxiety and depressive symptoms in the general population was recorded during the lockdown. In April 2020, an 86-year-old woman was admitted to the Coronary Intensive Care Unit of our hospital. Her remote medical history shows: arterial hypertension, previous breast cancer, operated and treated with adjuvant radiotherapy and hormone therapy, and cervical cancer, subjected to radical hysterectomy and subsequent pelvic radiotherapy. Upon entering the ward, the patient was in a state of shock (BP 75/50 mmHg, HR 105/m') and there was marked hypothermia (34 °C). The relatives reported that the patient did not leave home since the beginning of the Sars-CoV-2 pandemic due to the high fear of contracting the infection and in the day before admission she had a feverish rise (39 °C), which regressed spontaneously. ECG showed sinus tachycardia with ST-segment elevation V2–V6, in I and aVL and under level in III and aVR (Figure 1) with elongated QT interval. Echocardiogram revealed akinesia of the mid-apical segments, with kinetics preserved in the basal segments, severe left ventricular systolic dysfunction (ejection fraction: 25%), moderate dual-jet mitral insufficiency due to symmetrical tethering of the flaps and a mild infero-lateral pericardial effusion. The indices of myocardionecrosis and inflammation were high. The patient was asymptomatic for chest pain and equivalents and expressed an excessive fear of having contracted COVID-19. Nasal swab for SARS-CoV-2 was performed, which was negative. The interTAK score was 68 (Takotsubo probability: 82.4%). Emergency coronary angiography was performed, which showed no critical coronary stenosis. Ventriculography revealed apical dyskinesia with hyperkinesis of the basal segments (Figure 2). At the end of the procedure due to hemodynamic instability an intra-aortic balloon pump (IABP) was placed and inotropic and vasopressor therapy was undertaken. Over the next 48 h there were numerous episodes of non-sustained ventricular tachycardia and amiodarone was applied for the onset of atrial fibrillation, with prompt restoration of the sinus rhythm. The patient was progressively weaned from the mechanical and pharmacological support of the circulation and she was discharged in optimal medical therapy, with indication for echocardiographic follow-up, still in progress.

scholarly journals EFFECT OF PREHOSPITAL SYSTEMIC THROMBOLYSIS ON LEFT VENTRICULAR SYSTOLIC DYSFUNCTION IN ST-SEGMENT ELEVATION ACUTE MYOCARDIAL INFARCTION

2021 ◽  
Vol 14 (3) ◽  
Author(s):  
A Alavi ◽  
S Kenzhaev ◽  
I Kakharov
Keyword(s):  
Standard Therapy ◽  
Left Ventricular Systolic Dysfunction ◽  
Myocardial Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Control Group ◽  
Ventricular Systolic Dysfunction ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
St Segment

Objective: to study the effect of prehospital thrombolysis on left ventricular systolic dysfunction in patients with acute ST-segment elevation coronary syndrome.Material and methods: The study included 70 patients with acute coronary syndrome with ST-segment elevation. Patients were randomized into two groups: control (group A) - 35 patients receiving standard therapy, and hospital TLT. Group B included 35 patients who underwent standard therapy and prehospital TLT. All 70 patients underwent echocardiography 1 day after myocardial revascularization and 3 months later.Results: the use of early myocardial reperfusion in patients with STEMI had a positive effect on central hemodynamics, reduced the development of LV volume overload, as a result of which end-diastolic and systolic volumes did not change during 3 months of follow-up. LVEF grew in both groups, and its growth was more pronounced in group B.Conclusion: timely prehospital reperfusion reduces the severity of myocardial damage and thus prevents the development of severe systolic myocardial dysfunction LV.

scholarly journals Assessment of Selected Baseline and Post-PCI Electrocardiographic Parameters as Predictors of Left Ventricular Systolic Dysfunction after a First ST-Segment Elevation Myocardial Infarction

2021 ◽  
Vol 10 (22) ◽  
pp. 5445
Author(s):  
Tomasz Fabiszak ◽  
Michał Kasprzak ◽  
Marek Koziński ◽  
Jacek Kubica
Keyword(s):  
Myocardial Infarction ◽  
Regression Analysis ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Ventricular Systolic Dysfunction ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Qrs Duration

Objective: To assess the performance of ten electrocardiographic (ECG) parameters regarding the prediction of left ventricular systolic dysfunction (LVSD) after a first ST-segment-elevation myocardial infarction (STEMI). Methods: We analyzed 249 patients (74.7% males) treated with primary percutaneous coronary intervention (PCI) included into a single-center cohort study. We sought associations between baseline and post-PCI ECG parameters and the presence of LVSD (defined as left ventricular ejection fraction [LVEF] ≤ 40% on echocardiography) 6 months after STEMI. Results: Patients presenting with LVSD (n = 52) had significantly higher values of heart rate, number of leads with ST-segment elevation and pathological Q-waves, as well as total and maximal ST-segment elevation at baseline and directly after PCI compared with patients without LVSD. They also showed a significantly higher prevalence of anterior STEMI and considerably wider QRS complex after PCI, while QRS duration measurement at baseline showed no significant difference. Additionally, patients presenting with LVSD after 6 months showed markedly more severe ischemia on admission, as assessed with the Sclarovsky-Birnbaum ischemia score, smaller reciprocal ST-segment depression at baseline and less profound ST-segment resolution post PCI. In multivariate regression analysis adjusted for demographic, clinical, biochemical and angiographic variables, anterior location of STEMI (OR 17.78; 95% CI 6.45–48.96; p < 0.001), post-PCI QRS duration (OR 1.56; 95% CI 1.22–2.00; p < 0.001) expressed per increments of 10 ms and impaired post-PCI flow in the infarct-related artery (IRA; TIMI 3 vs. <3; OR 0.14; 95% CI 0.04–0.46; p = 0.001) were identified as independent predictors of LVSD (Nagelkerke’s pseudo R2 for the logistic regression model = 0.462). Similarly, in multiple regression analysis, anterior location of STEMI, wider post-PCI QRS, higher baseline number of pathological Q-waves and a higher baseline Sclarovsky-Birnbaum ischemia score, together with impaired post-PCI flow in the IRA, higher values of body mass index and glucose concentration on admission were independently associated with lower values of LVEF at 6 months (corrected R2 = 0.448; p < 0.00001). Conclusions: According to our study, baseline and post-PCI ECG parameters are of modest value for the prediction of LVSD occurrence 6 months after a first STEMI.

scholarly journals Role of Cardiac Troponin I level in predicting in-hospital outcomes in patients with ST-segment elevation myocardial infarction in Erbil-Iraq

2016 ◽  
Author(s):  
Salam Zangana ◽  
Abdulkareem Al-Othman ◽  
Namir Al-Tawil
Keyword(s):  
Myocardial Infarction ◽  
Troponin I ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Troponin Level ◽  
Hospital Outcomes ◽  
St Segment Elevation ◽  
St Segment

Background and objectives: The correlation of cardiac troponin I with early in-hospital outcomes in acute myocardial infarction is not well established. This study aims to assess the role of troponin I in predicting in-hospital outcomes and early left ventricular systolic dysfunction in patients with ST-segment elevation myocardial infarction (STEMI). Patients and methods: In a prospective study, 116 patients (74males and 42 females), with STEMI who had been admitted to the Coronary CareUnit from March 2015 to September 2015 were enrolled. Patients were divided according to the level of troponin I on admission into 3 groups (low, medium and high elevation). Results: The mean age (+ SD) of the patients was 60+11.4 years. The troponin level of 66.2% of males was high compared with 52.4% of females (p=0.002). The incidence of acute pulmonary edema (21.1%), cardiogenic shock (7%) and early left ventricular systolic dysfunction (49.3%) was significantly higher among patients with high troponin level compared with (0%, 0% and 16%, respectively) among patients with low troponin level. All deaths and cardiac arrest were of high troponin level. Conclusions: High admission troponin I in STEMI permits early identification of patients at increased risk of major cardiac complications and death.

scholarly journals Left Ventricular Systolic Dysfunction Caused by the Fistula from the Aortic Graft Pseudoaneurysm to the Left Ventricle

2020 ◽  
Vol 50 (6) ◽  
pp. 536
Author(s):  
İsmail Balaban ◽  
Ahmet Karaduman ◽  
Berhan Keskin ◽  
Semih Kalkan ◽  
Dogancan Ceneli ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Aortic Graft ◽  
Ventricular Systolic Dysfunction

scholarly journals Enhanced Inflammation is a Marker for Risk of Post-Infarct Ventricular Dysfunction and Heart Failure

2020 ◽  
Vol 21 (3) ◽  
pp. 807 ◽  
Author(s):  
Iwona Świątkiewicz ◽  
Przemysław Magielski ◽  
Jacek Kubica ◽  
Adena Zadourian ◽  
Anthony N. DeMaria ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Multivariable Analysis ◽  
High Sensitivity ◽  
Left Ventricular ◽  
St Segment Elevation ◽  
Reactive Protein

Acute ST-segment elevation myocardial infarction (STEMI) activates inflammation that can contribute to left ventricular systolic dysfunction (LVSD) and heart failure (HF). The objective of this study was to examine whether high-sensitivity C-reactive protein (CRP) concentration is predictive of long-term post-infarct LVSD and HF. In 204 patients with a first STEMI, CRP was measured at hospital admission, 24 h (CRP24), discharge (CRPDC), and 1 month after discharge (CRP1M). LVSD at 6 months after discharge (LVSD6M) and hospitalization for HF in long-term multi-year follow-up were prospectively evaluated. LVSD6M occurred in 17.6% of patients. HF hospitalization within a median follow-up of 5.6 years occurred in 45.7% of patients with LVSD6M vs. 4.9% without LVSD6M (p < 0.0001). Compared to patients without LVSD6M, the patients with LVSD6M had higher CRP24 and CRPDC and persistent CRP1M ≥ 2 mg/L. CRP levels were also higher in patients in whom LVSD persisted at 6 months (51% of all patients who had LVSD at discharge upon index STEMI) vs. patients in whom LVSD resolved. In multivariable analysis, CRP24 ≥ 19.67 mg/L improved the prediction of LVSD6M with an increased odds ratio of 1.47 (p < 0.01). Patients with LVSD6M who developed HF had the highest CRP during index STEMI. Elevated CRP concentration during STEMI can serve as a synergistic marker for risk of long-term LVSD and HF.

Is everything clear about Tako-Tsubo syndrome?

Folia Medica ◽  
2011 ◽  
Vol 53 (2) ◽  
pp. 5-35 ◽  
Author(s):  
Ivo S. Petrov ◽  
Mariya P. Tokmakova ◽  
Daniel N. Marchov ◽  
Kostadin N. Kichukov
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Systolic Dysfunction ◽  
Systolic Dysfunction ◽  
Clinical Manifestations ◽  
Apical Ballooning ◽  
Microvascular Dysfunction ◽  
Good Prognosis ◽  
Acute Onset ◽  
Left Ventricular ◽  
Catecholamine Excess

Abstract Introduction: Tako-tsubo syndrome is a novel cardio-vascular disease affecting predominantly postmenopausal women exposed to unexpected strong emotional or physical stress, in the absence of significant coronary heart disease. It is characterized by acute onset of severe chest pain and/or acute left ventricular failure, ECG-changes, typical left ventricular angiographic findings, good prognosis and positive resolution of the morphological and clinical manifestations. First described in 1990 in Japan by Sato, Tako-tsubo cardiomyopathy is characterized by transient contractile abnormalities of the left ventricle, causing typical left ventricular apical ballooning at end-systole with concomitant compensatory basal hyperkinesia. There are also atypical forms, presenting with left ventricular systolic dysfunction which affects the mid-portions of the left ventricle. The etiology of the disease still remains unclear. Many theories have been put forward about the potential underlying pathophysiological mechanisms that may trigger this syndrome among which are the theory of catecholamine excess, the theory of multivessel coronary vasospasm, the ischemic theory, and the theory of microvascular dysfunction and dynamic left ventricular gradient induced by elevated circulating catecholamine levels. Adequate management of Tako-tsubo syndrome demands immediate preparation for coronary angiography. Once the diagnosis is made, treatment is primarily symptomatic and includes monitoring for complications. Patients with Tako-tsubo syndrome most frequently develop acute LV failure, pulmonary edema, rhythm and conductive disturbances and apical thrombosis. Treatment is symptomatic and includes administration of diuretics, vasodilators and mechanical support of circulation with intra-aortic balloon counterpulsation.

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