Abstract Introduction Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and a major preventable cause of stroke. The diagnosis of AF on electrocardiogram is through the recognition of absent p waves and an irregularly irregular ventricular rhythm. However, in ventricular-paced patients, the rhythm on electrocardiogram (ECG) is often regular and may obscure AF diagnosis. Thus, unrecognized AF on ECG poses a potential risk among untreated ventricular-paced patients. There is scant published data reporting the prevalence of underrecognized and untreated ECG-detected AF among ventricular-paced patients. Objectives In the first part of this study, we aim (1) to determine the prevalence of AF and unreported AF on ECGs with ventricular-paced rhythm obtained across all 6 hospitals in our city, Canada. Using data obtained from (1), we then aim (2) to report the rates of untreated and unreported ECG-detected AF among ventricular-paced patients with an indication for anticoagulation, (3) to describe the length of delay in AF recognition and treatment among patients who should be considered for anticoagulation at the time of ECG-detected AF and (4) to identify possible strategies that can improve reporting of AF on ECGs with ventricular-paced rhythm using our institutional ECG software. Methods This is a retrospective multicenter review of ventricular-paced ECGs interpreted and reported by physicians using our institutional ECG software. ECGs were reviewed and confirmed by two independent cardiologists who were blinded from the reported interpretation of the ECGs. Results Of the sample of 1500 ECGs with ventricular-paced rhythm from 2017–2019, 2 independent cardiologists agreed that AF was present in 622 ECGs (41.5%). Of these, 251 (40.4%) were not reported to have AF by the interpreting physician. Conclusions Our study shows that there is a high prevalence of unreported AF on ECG in patients with ventricular-paced rhythm in our local hospitals. Further studies are warranted on describing whether this impacts treatment and outcomes among ventricular-paced patients. This study also highlights the importance of identifying possible strategies to improve reporting of AF on ECGs with ventricular-paced rhythm. Funding Acknowledgement Type of funding sources: None.
Tako-Tsubo cardiomyopathy (TTC), also known as transient left ventricular apical ballooning syndrome,1 is a reversible, stress-induced cardiomyopathy that predominantly affects post-menopausal, elderly women during emotional or physical stress.1,2 Although it is an increasingly recognized and reported syndrome, the syndrome remains uncommon, occurring in <1% of patients referred for coronary angiogram.
A 74-year-old male with known pulmonary fibrosis, follicular lymphoma, sleep apnea, and truncal obesity, reported progressive exertional dyspnea. During a 6-minute walk test, his oxygen saturation dropped from 94% to 86% postexercize. CT chest suggested subpleural reticulation with ground-glass opacities; dilated ascending aorta and root (both 41 mm), and resultant compressed right atrium (RA) (Figure 1A). A VQ scan did not identify any significant perfusion defect. His hemoglobin was 180 g/L (hematocrit-51%). Transthoracic echocardiography demonstrated a positive bubble test, both at rest and post-Valsalva maneuver (Supplemental Video 1). A transesophageal echocardiogram confirmed compressed RA characterized by reduced distance between the limbus and the posterior wall of the atrium (Figure 1B, C). His mean RA and LA pressures were 6- and 15 mm Hg respectively. Bilateral pulmonary venous saturation was 95% to 96%, whereas the aortic saturation was 91% suggestive of intracardiac right-to-left shunt. Superior and inferior vena cava (IVC) angiograms demonstrated opacification of the RA, RV, and pulmonary artery, without any significant shunting through a patent foramen ovale (PFO) (Supplemental Videos 2 and 3, Figure 1D, E). As the intracardiac shunt was suspected, we performed a hepatic venogram that demonstrated right-to-left shunt through the PFO (Figure 1F, Supplemental Video 4). Transcatheter closure of a PFO using a 30 mm Gore PFO occluder device eliminated the shunt and normalized systemic saturation. The in-utero IVC just below the diaphragm receives blood from the following: (1) the distal inferior vena cava, (2) the ductus venosus, (3) the portal vein, and (4) the hepatic veins, each with different oxygen saturations. In contrast to the general belief that there is an adequate mixture of this blood in the cephalic portion of the IVC, it is preferentially the highly oxygenated ductus venosus blood that selectively streams through the foramen ovale,1Edelstone D.I. Rudolph A.M. Preferential streaming of ductus venosus blood to the brain and heart in fetal lambs.Am J Physiol. 1979; 237: H724-H729https://doi.org/10.1152/ajpheart.1979.237.6.H724Crossref PubMed Google Scholar whereas the IVC flow enters into the right ventricle. In adults, hepatic vein drains ∼25% to 30% of the total cardiac output; hepatic venous saturation is lower than that from superior vena cava and IVC. Altered geographical relationships between venous drainages and cardiac structures can create a "perfect storm" allowing streaming of venous flow through a PFO. Although this patient had pulmonary fibrosis, careful workup identified a PFO-mediated right-to-left shunt. Transcatheter closure resolved systemic desaturation. This is the first case describing the role of hepatic venous flow in PFO-mediated right-to-left shunting and systemic desaturation. •PFO commonly produces intermittent right-to-left shunting due to episodic elevation of RA pressure.•Altered anatomic relationships between venous drainages and cardiac structures can induce PFO shunting.•In the setting of novel pathoanatomic conditions, redirected hepatic vein flow can cause R-L shunting through a PFO. The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. This work was not supported by funding agencies in the public, commercial, or not-for-profit sectors.
Abstract Background:Although the 12‐lead electrocardiogram (ECG) has been found useful in identifying the left anterior descending (LAD) coronary artery as the infarct‐related artery in acute myocardial infarction (MI), it has traditionally been felt to be incapable of localizing the culprit lesion within the LAD itself. Such a capability would be important, because anterior MI due to proximal LAD lesions carry a much worse prognosis than those due to more distal or branch vessel lesions. Hypothesis:This study investigated whether certain ECG variables—especially an ST‐segment injury pattern in leads aVL and/or V 1 —would correlate with culprit lesion site, and an ECG algorithm was developed to predict culprit lesion site. Methods:The initial ECGs of 55 patients who had undergone cardiac catheterization after an anterior or lateral MI were reviewed to identify the leads with an ST‐segment injury pattern; the corresponding catheterization films were then reviewed to identify the location of the culprit lesion; and these separate findings were then compared. Results:The sensitivity and specificity of an ST‐injury pattern in a VL in predicting a culprit lesion before the first diagonal branch were 91 and 90%, respectively; the same values in predicting a lesion prior to the first septal branch were 85 and 78%. ST‐segment elevation in V 1 , on the other hand, was a much less sensitive and specific predictor of a preseptal lesion. Overall, our algorithm correctly identified the culprit lesion location in 82% of our patients. Conclusion:Based on our findings, we conclude that an ST‐segment injury pattern in a VL during an anterior myocardial infarction predominantly reflects a proximal LAD lesion and therefore constitutes a high‐risk finding.
Abnormal atrial depolarization, characterized by P waves ≧110 ms on the electrocardiogram, can manifest as partial or advanced interatrial conduction delay or interatrial block (IAB). Progression from partial to advanced IAB has been shown to be altered by the use of angiotensin-converting enzyme inhibitors and β-adrenergic blockers. We previously reported that advanced IAB, denoted by biphasic P waves in leads II, II and aVF, can revert intermittently to its partial counterpart. However, potential factors that could induce such resolution remain unknown. We present the first known case of resolution of advanced IAB to partial IAB occurring during graded exercise, following treatment with a β-adrenergic blocker. Only continued study of these and other novel factors will help us understand the exact pathophysiology of both, partial and advanced IAB.
