scholarly journals Methadone-Induced Polymorphic Ventricular Tachycardia Complicated by Takotsubo Cardiomyopathy in a Malnourished Patient

2021 ◽  
Vol 9 ◽  
pp. 232470962110051
Author(s):  
Mohammed Ali ◽  
Omeralfaroug Adam ◽  
Ahmed Subahi ◽  
Abdalaziz Awadelkarim ◽  
Lubna Fatiwala ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Coronary Disease ◽  
Takotsubo Cardiomyopathy ◽  
Myocardial Dysfunction ◽  
Polymorphic Ventricular Tachycardia ◽  
Malnourished Patient

Takotsubo cardiomyopathy (TC) is a syndrome characterized by acute and transient regional systolic myocardial dysfunction. TC often mimics myocardial infarction without obstructive coronary disease. We present a case of a 48-year-old woman who developed TC following the onset of polymorphic ventricular tachycardia in the setting of methadone intoxication.

scholarly journals Mode of onset of polymorphic ventricular tachycardia in acute myocardial infarction

2010 ◽  
Vol 26 (7) ◽  
pp. e254-e257 ◽  
Author(s):  
Bulent Gorenek ◽  
Osman Cengiz ◽  
Gulmira Kudaiberdieva ◽  
Ilker Durak ◽  
Volkan Dogan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia

scholarly journals Mapping and ablation of polymorphic ventricular tachycardia after myocardial infarction

2004 ◽  
Vol 44 (8) ◽  
pp. 1700-1706 ◽  
Author(s):  
Lukasz Szumowski ◽  
Prashanthan Sanders ◽  
Franciszek Walczak ◽  
Mélèze Hocini ◽  
Pierre Jaïs ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia

scholarly journals -272-EPICARDIAL MAPPING OF INDUCED NONSUSTAINED POLYMORPHIC VENTRICULAR TACHYCARDIA IN CANINE MYOCARDIAL INFARCTION

1986 ◽  
Vol 50 (6) ◽  
pp. 539-540
Author(s):  
SATOSHI OGAWA ◽  
TOSHIHISA MIYAZAKI ◽  
TAKASHI SAKAI ◽  
MICHlYO HOSOKAWA ◽  
KENJI SAKURAI ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Polymorphic Ventricular Tachycardia ◽  
Epicardial Mapping ◽  
Canine Myocardial Infarction

Polymorphic ventricular tachycardia and abnormal Ca2+ handling in very-long-chain acyl-CoA dehydrogenase null mice

2007 ◽  
Vol 292 (5) ◽  
pp. H2202-H2211 ◽  
Author(s):  
Andreas A. Werdich ◽  
Franz Baudenbacher ◽  
Igor Dzhura ◽  
Loice H. Jeyakumar ◽  
Prince J. Kannankeril ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Sarcomere Length ◽  
Myocardial Dysfunction ◽  
Time Derivative ◽  
Polymorphic Ventricular Tachycardia ◽  
Chain Acyl ◽  
Intracellular Ca ◽  
Current Characteristics ◽  
Isoproterenol Infusion ◽  
Long Chain

Patients with mutations in the mitochondrial very-long-chain acyl-CoA dehydrogenase (VLCAD) gene are at risk for cardiomyopathy, myocardial dysfunction, ventricular tachycardia (VT), and sudden cardiac death. The mechanism is not known. Here we report a novel mechanism of VT in mice lacking VLCAD (VLCAD−/−). These mice exhibited polymorphic VT and increased incidence of VT after isoproterenol infusion. Polymorphic VT was induced in 10 out of 12 VLCAD−/− mice (83%) when isoproterenol was used. One out of 10 VLCAD−/− mice with polymorphic VT had VT with the typical bidirectional morphology. At the molecular level, VLCAD−/− cardiomyocytes showed increased levels of cardiac ryanodine receptor 2, phospholamban, and calsequestrin with increased [3H]ryanodine binding in heart microsomes. At the single cardiomyocyte level, VLCAD−/− cardiomyocytes showed significant increase in diastolic indo 1 and fura 2 fluorescence, with increased Ca2+ transient amplitude. These changes were associated with altered Ca2+ dynamics, to include: faster sarcomere contraction, larger time derivative of the upstroke, and shorter time-to-minimum sarcomere length compared with VLCAD+/+ control cells. The L-type Ca2+ current characteristics were not different under voltage-clamp conditions in the two VLCAD genotypes. Sarcoplasmic reticulum Ca2+ load measured as normalized integrated Na+/Ca2+ exchange current after rapid caffeine application was increased by 48% in VLCAD−/− cells. We conclude that intracellular Ca2+ handling represents a possible molecular mechanism of arrhythmias in mice and perhaps in VLCAD-deficient humans.

scholarly journals Recurrent Postmyocardial Infarction Ventricular Tachycardia: An Unusual Culprit

2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Akhil Kumar Sharma ◽  
Nirdesh Jain ◽  
Safal Safal ◽  
Vikas Kumar ◽  
Sudhanshu Kumar Dwivedi
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Ventricular Fibrillation ◽  
Coronary Angiography ◽  
Polymorphic Ventricular Tachycardia ◽  
Inferior Wall ◽  
Postmyocardial Infarction ◽  
Life Saving ◽  
Pacing Lead ◽  
Multiple Episodes

Although temporary transvenous pacing is life-saving in patients with myocardial infarction who develop bradyarrhythmias, the electrical complications resulting from it can be fatal and are rarely reported. We report here a patient with acute inferior wall myocardial infarction who required temporary transvenous pacing due to second-degree atrioventricular block accompanied with hypotension. Following coronary angiography and successful revascularisation, the patient developed multiple episodes of monomorphic and polymorphic ventricular tachycardia as well as ventricular fibrillation which on careful inspection were found to be initiated by fusion of the intrinsic and paced complexes. The problem of malignant ventricular tachycardia was solved by simple removal of the pacing lead. To the best of our knowledge, malignant ventricular tachycardia of both monomorphic and polymorphic types initiated by fusion complexes in a paced patient has not been reported in literature.

Artifact mimicking non-sustained polymorphic ventricular tachycardia in a patient with recent myocardial infarction

Open Medicine ◽  
2010 ◽  
Vol 5 (2) ◽  
pp. 154-155
Author(s):  
Gökmen Gemici ◽  
Ali Kalkan ◽  
Muzaffer Degertekin ◽  
Ertan Demirtas
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Tachycardia ◽  
Cycle Length ◽  
Coronary Care Unit ◽  
Polymorphic Ventricular Tachycardia ◽  
Recent Myocardial Infarction ◽  
Wide Complex Tachycardia ◽  
History Of ◽  
Coronary Care ◽  
Ecg Abnormalities

AbstractA 78-year-old woman with a history of recent myocardial infarction was admitted to the coronary care unit because of dyspnea. The baseline ECG revealed sinus rhythm of 90 beats/min. Two hours after her admission, her body temperature raised to 38.8 degrees Celcius accompanied by shaking chills. Wide complex tachycardia runs consistent with polymorphic ventricular tachycardia synchronous with shaking chills were noticed on the monitor. Closer observation of the ECG revealed the presence of normal QRS complexes at the cycle length of baseline rhythm. It was presumed that artifact due to shaking chills was responsible for the ECG abnormalities.

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