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Tako-tsubo cardiomyopathy is a relatively recently recognized clinical entity, which presents similar to an acute myocardial infarction but there is no evidence of obstructive coronary artery disease on cardiac catheterization. It mostly affects postmenopausal women and an episode of acute illness or stress can often be identified preceding the presentation. Tako-tsubo cardiomyopathy (TCM) usually has a favorable outcome and an excellent prognosis but, in rare instances, it can be associated with life threatening complications. We report a unique case of TCM where the patient presented with a transient complete heart block., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Introduction:  Takotsubo cardiomyopathy (TC) is a unique transient nonischemic cardiomyopathy that mimics acute myocardial infarction (MI). The aim of our study was to evaluate electrocardiographic changes in patients with TC, including the frequency of ST elevation and other abnormalities., Methods:  Eleven patients were retrospectively identified from echocardiography database. All patients underwent coronary angiography and fulfilled the Mayo criteria for diagnosis of TC during the period November 2005 to September 2010. Standard 12-lead electrocardiograms recorded daily during the first week of hospitalization, after onset of symptoms were analyzed., Results:  Eight of 11 patients were found to have ST elevation, of which two patients had ST depression in reciprocal leads. No patient had ST elevation in lead V1, most likely reason being that wall-motion abnormalities in TC rarely extend to the region faced by lead V1. Pathological Q waves were found in five patients, of which two patients had transient Q waves, suggesting less myocardial damage. All 11 patients had T-wave inversion; eight of these patients had diffuse symmetric T-wave inversion, extending beyond the perfusion territory of any single coronary artery. QTc interval prolongation was found in 10 patients. All patients had left ventricular ejection fraction between 25% and 35% on presentation, which could not be predicted by the extent of electrocardiogram (ECG) changes., Conclusion:  ECG changes in TC are distinctive and differ from those typically seen in acute anterior MI. The ECG abnormalities described may be important clues for the clinician to suspect diagnosis of TC in the right clinical setting., (©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc.)

Background: Acute coronary syndrome (ACS) resulting from culprit lesion in left main coronary artery (LMCA) can cause rapid hemodynamic deterioration. It is important to identify these patients early to facilitate timely revascularization. ST segment elevation in aVR greater than or equal to V(1) (aVR-V(1)>or= 0) has been suggested as a sensitive predictor of LMCA disease. As a result of balanced forces, we hypothesized that ST deviation in V(6) greater than or equal to ST deviation in V(1) (V(6)-V(1)>or= 0) might be a good determinant of LMCA disease., Methods: We compared admission 12-lead ECGs of ACS resulting from culprit LMCA lesion (n = 75, group I) with ACS resulting from culprit left anterior descending lesion (n = 81, group II). Group I was selected over a period of 10 years. We compared V(6)-V(1)>or= 0 to aVR-V(1)>or= 0 in both groups. We also looked at ratios of ST deviations in V(6),V(1) (V(6)/V(1)>or= 1) and aVR,V(1) (aVR/V(1)>or= 1) in patients where ST segment in V(1) was not isoelectric (group I = 54 and group II = 55)., Results: ST deviation in V(6) was significantly greater in group I as compared to group II (P < 0.001). The reliabilities of V(6)-V(1)>or= 0, V(6)/V(1)>or= 1, aVR-V(1)>or= 0, and aVR/V(1)>or= 1 in predicting LMCA disease were determined., Conclusion: This is the largest series of ECG analysis on ACS resulting from culprit LMCA lesion. V(6)-V(1)>or= 0 and V(6)/V(1)>or= 1 were more sensitive in predicting LMCA as culprit vessel in comparison to previously reported greater ST segment elevation in aVR than V(1).

We have observed an electrocardiographic (ECG) pattern of deep T-wave or "giant T wave" inversion in patients with acute coronary insufficiency. We reviewed the ECGs of 936 patients admitted to our coronary care unit during a one-year period. We found the pattern of giant T-wave inversion was present in nine patients (1 percent). We examined the echocardiograms of all of these patients and we analyzed the coronary angiograms on the seven patients in whom it was performed. We found that giant T-wave inversion was usually found in patients with stenosis in the left coronary system. In addition, the majority of these patients also had echocardiographic evidence of left ventricular hypertrophy. We conclude that the high frequency of a partially patent vessel in the left coronary system suggests that this ECG pattern may be useful in identifying patients who might benefit from coronary revascularization.

This study examines the relationship between QRS width and the presence of neoplasia. The QRS width was measured in 236 consecutive ambulatory patients. The patients' body surface area, CBC, SMA 6, and SMA 12 were also recorded. There were 17 out of 34 (50%) patients with neoplasia in the group with QRS less than 0.08 seconds. There were only 19 out of 78 (24%) with neoplasia in the group with QRS greater than or equal to 0.08 seconds (P less than 0.01). We conclude that there is a higher incidence of neoplasia in patients with a QRS less than 0.08 seconds than in patients with a QRS greater than or equal to 0.08 seconds. This difference cannot be explained by age, body surface area, hemoglobin, or any variable in SMA 6 or SMA 12.

This study follows patients with severe sinus bradycardia (40 beats per minute for 6 seconds or greater) in order to evaluate mortality and the effectiveness of permanent pacemaker insertion. Severe sinus bradycardia was noted on a 24-hour Holter in 95 patients. There were 64 males and 31 females with a mean age of 69 +/- 10 years. All were available for follow-up at 26 +/- 13 months. Twenty-eight required a permanent pacemaker at an average of 2 +/- 3 months after the Holter. Of this group 12 had the Holter for arrhythmia, 11 for cerebral symptoms, 4 for palpitations and 1 for chest pain. Only 1 was taking digitalis and no patients were taking Inderal. Six (21%) died at a mean interval of 21 +/- 15 months following pacemaker insertion. Sixty-seven did not require pacemaker insertion. The indications for Holter monitoring were arrhythmia in 16, palpitations in 19, cerebral symptoms in 20 and chest pain in 12. Four of these patients were on digitalis, 8 on Inderal, and 4 on both. Eleven (16%) died at a mean interval of 12 +/- 7 months after the initial Holter recording. Dizziness and/or syncope reoccurred in 22. Five had these symptoms even after pacemaker insertion. We conclude that severe sinus bradycardia is associated with a significant mortality. Insertion of a permanent pacemaker may decrease recurrent symptoms and slightly increase time of survival, but does not appear to influence the overall survival rate.

Controversy persists regarding the presence and extent of right ventricular involvement with acute anterior injury. Also unclear are the incidence and significance of ST elevations in the right-sided leads in acute left anterior descending artery occlusion. Baseline and coronary occlusion hemodynamics and 15-lead electrocardiograms (addition of RV3 through RV5) were recorded in 42 patients during 32 left anterior descending and 13 right coronary artery angioplasties. The right coronary and left anterior descending artery angioplasties had similar baseline right and left ventricular hemodynamics, as well as identical right atrial to pulmonary wedge pressure ratios (0.51 right coronary vs 0.51 left anterior descending). Whereas the right coronary and left anterior descending occlusions produced similar elevations in right ventricular filling pressures, the left anterior descending occlusions produced greater elevations in left ventricular filling pressures. The right atrial to pulmonary wedge ratio increased with right coronary occlusions, but was unchanged with left anterior descending occlusions (0.79 right vs 0.46 left, p less than or equal to 0.0001). Presence of right-lead ST elevations in 10 left anterior descending occlusions did not con-note increased right ventricular filling pressures, but did suggest increased left ventricular ischemia and dysfunction. In conclusion, right ventricular dysfunction, as manifested by increased filling pressures, is seen with both right coronary and left anterior descending occlusions. Although it is the predominant abnormality in right coronary occlusions, in left anterior descending occlusions it is proportional to left ventricular dysfunction. ST elevations in a right lead with left anterior descending occlusions do not constitute a marker for increased right ventricular dysfunction.