Sangshin Park, Min Kim, Dae In Lee, Ju-Hee Lee, Sangmin Kim, Sang Yeub Lee, Jang-Whan Bae, Kyung-Kuk Hwang, Dong-Woon Kim, Myeong-Chan Cho, Dae-Hwan Bae
Acute Crit Care. 2024;39(1):194-198. Published online May 11, 2022
The main mechanism of Takotsubo cardiomyopathy (TCM) is catecholamine-induced acute myocardial stunning. Pheochromocytoma, a catecholamine-secreting tumor, can cause several cardiovascular complications, including hypertensive crisis, myocardial infarction, toxic myocarditis, and TCM. A 29-year-old woman presented to our hospital with general weakness, vomiting, dyspnea, and chest pain. The patient was nullipara, 28 weeks’ gestation, and had a cachexic morphology. Her cardiac enzyme levels were elevated and bedside echocardiography showed apical akinesia, suggesting TCM. The next day, she could not feel the fetal movement, and an emergency cesarean section was performed. After delivery, the patient experienced cardiac arrest and was transferred to the intensive care unit for cardiopulmonary resuscitation (CPR). Spontaneous circulation returned after 28 minutes of CPR, but cardiogenic shock continued, and extracorporeal membrane oxygenation (ECMO) was initiated. On the third day of ECMO maintenance, left ventricular ejection fraction improved and blood pressure stabilized. On the eighth day after ECMO insertion, it was removed. However, complications of the left leg vessels occurred, and several surgeries and interventions were performed. A left adrenal gland mass was found on computed tomography and was removed while repairing the leg vessels. Pheochromocytoma was diagnosed and left adrenalectomy was performed.
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Background Patients with sepsis are at risk for developing sepsis-induced cardiomyopathy (SIC). Previous studies offer inconsistent results regarding the association of SIC and mortality. This study sought to assess whether SIC is linked to mortality in patients with sepsis and to evaluate predictors of the development of SIC.
Methods In this retrospective study, patients admitted to the medical intensive care unit with a diagnosis of sepsis in the absence of acute coronary syndrome were included. SIC was identified using transthoracic echo and was defined by a new onset decline in left ventricular ejection fraction (LVEF) ≤50%, or ≥10% decline in LVEF compared to baseline in patients with a history of heart failure with reduced ejection fraction. Multivariable logistic regression analysis was performed using the R software program.
Results Of the 359 patients in the final analysis, 19 (5.3%) had SIC. Eight (42.1%) of the 19 patients in the SIC group and 60 (17.6%) of the 340 patients in the non-SIC group died during hospitalization. SIC was associated with an increased risk for all-cause in-hospital mortality (odds ratio [OR], 4.46; 95% confidence interval [CI], 1.15–18.69; P=0.03). Independent predictors for the development of SIC were albumin level (OR, 0.47; 95% CI, 0.23–0.93; P=0.03) and culture positivity (OR, 8.47; 95% CI, 2.24–55.61; P=0.006). Concomitant right ventricular hypokinesis was noted in 13 (68.4%) of the 19 SIC patients.
Conclusions SIC was associated with an increased risk for all-cause in-hospital mortality. Low albumin level and culture positivity were independent predictors of SIC.
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Flexible bronchoscopy is a safe medical procedure, but the incidence rate of major complications is 0.08-0.3%. Here, we report 2 cases of stress induced cardiomyopathy, which developed immediately after flexible bronchoscopy. Stress related cardiomyopathy was confirmed by EKG, echocardiography, and coronary angiogram. The cardiac functions of these patients were fully recovered with conservative treatment. Although, the pathogenesis of stress related cardiomyopathy is not well understood, post-bronchoscopy tachycardia or arrhythmia is thought to be associated with hypoxemia or catecholamine excess. Because the clinical presentation is quite similar to acute myocardial infarction, discrete evaluations are required for appropriate treatment.
Stress-induced cardiomyopathy is a recently described acute and transient cardiomyopathy with typical left ventricular apical ballooning mimicking the clinical scenario of an acute myocardial infarction. Cesarean delivery causes intense emotional and physical stresses, which may precipitate stress-induced cardiomyopathy. We report a case presenting stress-induced cardiomyopathy occurring during ICU care in the early postpartum period following cesarean delivery.
Sung Gook Song, June Hong Kim, Kook Jin Chun, Jun Kim, Yong Hyun Park, Jeong Su Kim, Ju Hyun Park, Dong Cheul Han, Woo Hyun Cho, Doo Soo Jeon, Yun Seong Kim
Stress-induced cardiomyopathy (SICM) is an acute cardiac condition that causes left ventricular apical ballooning which mimicks acute coronary syndrome. The risk of in-hospital mortality with SICM is generally low (1% to 3%) and supportive care is usually sufficient for resolution.
Swine-origin influenza A (H1N1, S-OIV) is a recently spreading pandemic and a serious public health problem.
Although most S-OIV infections have a mild, self-limited course, clinical cases resulting in fatalities and associated with variable co-morbidities remain as a serious concern in some individuals. Among such serious complications, there have been few reports of SICM caused by S-OIV infection. We herein report, for the first time in the literature, a case with fatal hemodynamic instability secondary to SICM caused by S-OIV infection with viral pneumonia.
The major limitation to heart transplantation is the shortage of donor organs. In order to increase the cardiac donor pool, it is important to maintain stable hemodynamics and closely monitor cardiac function in cadaveric organ donors or potent donors. Recently, management of a potential cardiac donor pool has focused on aggressive hemodynamic management protocols and dobutamine stress echocardiography.
In our case, management with low dose dobutamine, glucose-insulin-potassium (GIK), and hormone therapy reversed heart failure following brain death and the heart was successfully transplanted. We suggest that aggressive hemodynamic management with low-dose dobutamine, GIK, and hormone therapy can result in the recruitment of more cadaveric hearts in marginal conditions.
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Predisposing Hemodynamic Factors Associated with a Failed Apnea Test during Brain Death Determination Eun Young Kim, Ji Hyun Kim The Korean Journal of Critical Care Medicine.2016; 31(3): 236. CrossRef
'Takotsubo cardiomyopathy' or 'stress-induced cardiomyopathy' is a newly described clinical entity that's characterized by transient left ventricular apical ballooning and left ventricular apical dyskinesis in the absence of any angiographic feature of significant coronary artery disease. The cause of takotsubo cardiomyopathy is unclear, but catecholamines probably play a role in the genesis of takotsubo cardiomyopathy. We report here on two cases of takotsubo cardiomyopathy that occurred during ICU care.
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Stress-induced Cardiomyopathy Following Cesarean Delivery with Hemorrhagic Shock - A Case Report - Youn Yi Jo, Ja Young Kwon, Yoon-Seong Jang, Yong Seon Choi The Korean Journal of Critical Care Medicine.2011; 26(1): 34. CrossRef
A 67-year old woman, hospitalized for the management of infectious colitis, developed acute congestive heart failure. Two-dimensional echocardiography revealed left ventricular apical akinesia (ballooning) and basal hyperkinesis, which was compatible with stress cardiomyopathy. A marked QT prolongation and T wave inversion followed by nonsustained polymorphic ventricular tachycardia was noted in the electrocardiogram. Intravenous administration of magnesium completely suppressed the ventricular tachycardia. After recovery from the colitis, the follow-up ECG and echocardiogram were normalized. There was no evidence of ischemic heart disease in the coronary angiography or perfusion scan. Takotsubo cardiomyopathy is one of the most important causes of acquired QT prolongation in ICU (intensive care unit) patients.. A careful monitoring of the QT interval in these patients is warranted particularly when drugs causing QT prolongation are used.
Intravenous immunoglobulin (IVIG) therapy has been introduced to idiopathic dilated cardiomyopathy due to their antiviral and anti-inflammatory effects. But each study reported conflicting result and treatment regimen has not been clearly established. We experienced a case of 28-year-old woman with idiopathic dilated cardiomyopathy with severely depressed cardiac function. Its onset time was obvious within 1 month. Despite of conservative treatment of heart failure, sudden cardiac arrest was developed. We tried IVIG therapy, and her symptoms and cardiac function were improved after IVIG treatment.
Peripartum cardiomyopathy (PPCM) is an unusual and uncommon causes of antepartum and postpartum heart failure, which may result in severe cardiac failure and death. PPCM is often unrecognized as symptoms of normal pregnancy commonly mimic those of mild heart failure but can rapidly progress to cardiac failure. We presented a case of elective labor induction in a patient with peripartum cardiomyopathy. A epidural analgesia technique was performed without difficulty for labor analgesia in parturient with peripartum cardiomyopathy. Her post-delivery course was uncomplicated but her baby has died due to respiratory failure. We suggest that vaginal delivery with careful incremental epidural alnalgesia in patient with PPCM is acceptable methods and close peripartum monitoring is essential in the management of PPCM.
Peripartum cardiomyopathy (PPCM) is defined as the onset of acute heart failure without demonstrable cause in the last trimester of pregnancy or within the first 6 months after delivery. Mortality from PPCM ranges from 25% to 50% and cause of death is usually chronic congestive heart failure or thromboembolic complications. We experienced 2 patients with PPCM. One was a twin pregnant woman and PPCM was developed after cesarean section. In the other case, PPCM was combined with aspiration pneumonia in the preterm labor patient. They were treated with diuretics and cardiotonic drugs and recovered to normal cardiac function within 7 to 10 days. Prognosis is related to recovery of left ventricular function, which usually occurs within 6 months postpartum. Early diagnosis and appropriate treatment of PPCM improve outcome.