Vinod K. Chaubey

Interatrial Block in the Modern Era

Interatrial block (IAB; P-wave duration ≥ 110 ms), which represents a delay in the conduction between the atria, is a pandemic conduction abnormality that is frequently underappreciated in clinical practice. Despite its comprehensive documentation in the medical literature, it has still not received adequate attention and also not adequately described and discussed in most cardiology textbooks. IAB can be of varying degrees and classified based on the degree of P-duration and its morphology. It can transform into a higher degree block and can also manifest transiently. IAB may be a preceding or causative risk factor for various atrial arrhythmias (esp. atrial fibrillation) and also be associated with various other clinical abnormalities ranging from left atrial dilation and thromboembolism including embolic stroke and mesenteric ischemia. IAB certainly deserves more attention and prospective studies are needed to formulate a standard consensus regarding appropriate management strategies.

P-wave indices in patients with pulmonary emphysema: do P-terminal force and interatrial block have confounding effects?

Introduction Pulmonary emphysema causes several electrocardiogram changes, and one of the most common and well known is on the frontal P-wave axis. P-axis verticalization (P-axis > 60°) serves as a quasidiagnostic indicator of emphysema. The correlation of P-axis verticalization with the radiological severity of emphysema and severity of chronic obstructive lung function have been previously investigated and well described in the literature. However, the correlation of P-axis verticalization in emphysema with other P-indices like P-terminal force in V1 (Ptf), amplitude of initial positive component of P-waves in V1 (i-PV1), and interatrial block (IAB) have not been well studied. Our current study was undertaken to investigate the effects of emphysema on these P-wave indices in correlation with the verticalization of the P-vector. Materials and methods Unselected, routinely recorded electrocardiograms of 170 hospitalized emphysema patients were studied. Significant Ptf (s-Ptf) was considered ≥40 mm.ms and was divided into two types based on the morphology of P-waves in V1: either a totally negative (−) P wave in V1 or a biphasic (+/−) P wave in V1. Results s-Ptf correlated better with vertical P-vectors than nonvertical P-vectors (P = 0.03). s-Ptf also significantly correlated with IAB (P = 0.001); however, IAB and P-vector verticalization did not appear to have any significant correlation (P = 0.23). There was a very weak correlation between i-PV1 and frontal P-vector (r = 0.15; P = 0.047); however, no significant correlation was found between i-PV1 and P-amplitude in lead III (r = 0.07; P = 0.36). Conclusion We conclude that increased P-tf in emphysema may be due to downward right atrial position caused by right atrial displacement, and thus the common assumption that increased P-tf implies left atrial enlargement should be made with caution in patients with emphysema. Also, the lack of strong correlation between i-PV1 and P-amplitude in lead III or vertical P-vector may suggest the predominant role of downward right atrial distortion rather than right atrial enlargement in causing vertical P-vector in emphysema.

Opana ER abuse and thrombotic thrombocytopenic purpura (TTP)-like illness: a rising risk factor in illicit drug users

We report the case of a 22 year-old-woman who presented with upper extremity cellulitis secondary to an infiltration of illicit intravenous drug use. She confessed to the intravenous use of Opana ER (an extended release oral formulation of oxymorphone) which is an opioid drug approved only for oral use. She was found to have clinical evidence of profound thrombotic microangiopathy which resulted due to the intravenous use of Opana ER. She showed full clinical improvement after withholding drug and supportive clinical care. Recent report of Opana ER intravenous abuse was published from Tennessee county and has now been increasingly recognised as one of the causes of thrombocytopenia which mimicks clinically as thrombotic thrombocytopenic purpura. Physicians should be aware of this association as the lack of familiarity to this can pose serious management dilemmas for our patients (especially the polysubstance abusers).

Spodick’s Sign: A Helpful Electrocardiographic Clue to the Diagnosis of Acute Pericarditis

Re: Masek KP, Levis JT. ECG diagnosis: Acute pericarditis. Perm J 2013 Fall;17(4):e146. DOI: http://dx.doi.org/10.7812/TPP/13-044. Dear Editor, We read with great interest the work by Masek and Levis published in a recent issue of The Permanente Journal.1 They describe a classical electrocardiographic evolution of acute pericarditis. In the presented first electrocardiogram (ECG) of Stage I acute pericarditis, we would like to bring to the readers’ attention an interesting ECG finding: Spodick’s sign (Figure 1).2 This sign has been named after our University professor David Spodick, MD, a world-famous physician for his work on the pericardial diseases. It signifies to a downsloping TP segment in patients with acute pericarditis and is present in about 80% of the patients affected with acute pericarditis. The sign is often best visualized in lead II and lateral precordial leads. In addition, Spodick’s sign may also serve as an important distinguishing electrocardiographic tool between the acute pericarditis and acute coronary syndrome.3 PR-segment depression when used alone can sometimes be a masquerader, as it can be seen in both acute pericarditis and acute coronary syndrome. However, the presence of PR depression and Spodick’s sign is often a giveaway to the diagnosis.4,5 Figure 1. Electrocardiogram (ECG) of a 42-year-old man diagnosed with acute idiopathic/viral pericarditis. ECG represents Stage-1 pericarditis with diffuse PR-segment depression and ST segment elevation (except leads V1 and aVR where PR elevation is noted). Rhythm ... In Masek and Levis’s Figure 1 ECG (www.thepermanentejournal.org/issues/2013/fall/5537-acute-pericarditis.html), TP-segment downsloping is clearly apparent especially in leads II, V4-6 with near complete resolution after treatment with nonsteroidal anti-inflammatory drugs (Masek and Levis’s Figure 2 [www.thepermanentejournal.org/issues/2013/fall/5537-acute-pericarditis.html]).

Electrocardiographic impacts of lung resection

INTRODUCTION Electrocardiographic (ECG) changes accompanying lung resection have not been well investigated previously in a large controlled series of human adults. Thus, our current investigation was undertaken for a better understanding of the ECG changes associated with lung resection. MATERIALS AND METHODS Medical records of 117 patients who underwent lung resection (segmentectomy, lobectomy, or pneumonectomy) were reviewed. Their clinical course and ECGs were compared during early, intermediate and late postoperative course (<1 month, 1 month to 1 year and >1 year post-op respectively). RESULTS Patients in the acute postoperative phase had higher heart rate, increased maximum P-duration and P-dispersion, increased incidence of atrial arrhythmias and frequent ST-T changes. P-vector and QRS-vector were significantly affected after the lung resections; the correlation being most consistent between the anatomical displacements and the QRS-vector in the majority of patients. The axial shifts also demonstrated a characteristic temporal relationship after left pneumonectomy (a leftward deviation in the acute, normal or slight rightward deviation in the intermediate and a rightward deviation in the late postoperative course). The precordial R/S transition is often affected due to the mediastinal shifts and the ECGs in patients after left lung resection may simulate acute anteroseptal myocardial infarction due to a delayed R/S transition. CONCLUSION The understanding and recognition of the expected ECG findings after lung resection are imperative to avoid confusing these changes with other acute cardiopulmonary events which would prevent unnecessary further investigational work-up. These ECG changes are often dynamic and may bear a temporal relationship to the dynamic post-surgical changes in the thoracic anatomy.

Thyrotoxic hypercoagulable state with cerebral venous thrombosis and venous infarction masquerading as epilepsia partialis continua

A 42‐year‐old, female patient admitted to the emergency department with headache, altered mental status and convulsions. On examination, fever was 39.5°C, Glasgow Coma Scale score was 11 and signs of meningeal irritation were present. There was no hepatosplenomegaly. She had neurosurgical operations for cranial epidermoid tumor in 1989, 1998 and 2009. In 2011, she had ventriculoperitoneal shunt insertion for hydrocephalus and had shunt revision for shunt dysfunction 5 months before this admission. She had a history of animal livestock until 2010. Cranial computerized tomography revealed mild hydrocephalus. Cerebrospinal fluid (CSF) analysis revealed protein: >2 g/dl, glucose: 12 mg/dl (concomitant serum glucose level: 98 mg/dl) and 100 leukocytes/mm3. She was initiated on meropenem 2 gr q8h and vancomycin 500 mg q6h empirically. On the 3rd day of treatment, CSF culture yielded B. melitensis. Vancomycin and meropenem were stopped and ceftriaxone 2 gr q12 h, rifampicin 600 q24 h and doxycycline 100 mg q12 h were started. Serum Brucella agglutination tests were: Rose Bengal (+), Standard Wright 1/640 (+), 2‐mercapto‐ethanol test 1/640 (+), Rose Bengal test was (+) in the CSF. On day‐18 of treatment, repeated CSF showed 50 leukocytes/mm3. CSF analysis revealed Rose Bengal test (+) and Standard Wright: 1/320. Fever resolved on day‐5 of treatment. Neurosurgeons felt against change of the shunt. Three drug therapies were given for 6 weeks and the patient was discharged on rifampicin 600 q24 h and doxycycline 100 mg q 12 h for 6 month. There was no relapse during the follow‐up at 12 months.

Cost analysis of the History, ECG, Age, Risk factors, and initial Troponin (HEART) Pathway randomized control trial

We readwith great pleasure thework done by Riley et al. [1]. The authors have done commendable work to show that the HEART Pathway as a decision aid for patients with undifferentiated chest pain achieved cost savings. This would be of considerable value if replicated in routine clinical practice, given the burden of chest pain emergency room (ER) visits across the country [2]. We would like to share our concerns and thoughts on the cost analysis reported here and its implications. First, the authors chose to use a healthcare system perspective and not a societal perspectivewhich is typically the norm for economic evaluation [3]. If a societal perspective is considered, the scope of costs to be considered would be much broader, including those that accrue to patients directly, such as transportation costs. This is particularly relevant to a patient presenting with chest pain to the ER whomay be unable to receive care outside of this safety net setting owing to a variety of reasons. Second, although the original randomized controlled study only collected outcomes for 30 days, ideally the period of analysis (time horizon) for this cost analysis should be longer than 30 days. It is easy to imagine a situation where a patient in the HEART pathway was discharged early from the ER but was only able to obtain a primary care appointment 6 weeks from the ER visit. If a stress test was then ordered, this cost would not have been captured in this study. A time horizon of 6 months or 1 year would be more appropriate, with modeling of estimated costs for the purpose of the analysis. If cost-effectiveness is calculated, this would require modeling of outcomes as well. Third, the authors did not perform any sensitivity analysis which is typically

Ruptured Intracranial Lipoma—A Fatty Outburst in the Brain

Intracranial lipomas are rare congenital lesions that occur because of abnormal differentiation of embryogenic meninges. These lipomas are usually seen incidentally on brain imaging, and are usually asymptomatic and do not require treatment. The authors present a case of ruptured intracranial lipoma, discovered in an elderly patient presenting with dizziness and episodes of falls.

Takotsubo cardiomyopathy associated with perimyocarditis: yet another important differential diagnosis to entertain

Dear Sir, We read with great interest the report by Lee et al,(1) who did a commendable job of illustrating the clinical pearls in perimyocarditis and emphasised the importance of recognising its electrocardiographic evolution/staging. However, we would like to point out an additional important diagnostic electrocardiographic marker. In the first electrocardiogram (ECG) of Lee et al’s report,(1) downsloping of TP segments, known as Spodick’s sign,(2) which is named after the pioneer work of our former university professor Dr David Spodick, is observed. This finding is best noted in lead II and the lateral precordial leads, and is present in about 80% of cases of acute pericarditis (Fig. 1). It also serves as an excellent electrocardiographic tool for differentiating acute pericarditis from acute coronary syndrome. Fig. 1 Initial ECG (from Lee et al’s case report(1)) shows Spodick’s sign, which is the downsloping TP segments in lateral precordial leads, viz. V4, V6, and lead II (black arrows [inserted by current authors]). The electrocardiographic pattern observed in the second ECG, viz. convex tomb-stoning ST elevations with absence of PR segment depression, is unusual for the electrocardiographic evolution of pericarditis or perimyocarditis, though it may be observed (albeit rarely) in frank myocarditis or myopericarditis.(3) Since the diagnosis was based mostly on the clinical context, we wish to emphasise the importance of entertaining an alternate differential diagnosis or clinical explanation. The understanding of the pathophysiology and risk factors for takotsubo cardiomyopathy (TC) has been a continuously evolving process. The association between classical- or variant-form (regional) TC and perimyocarditis has been recognised recently and emphasised in one of our prior works.(4) The preceding myopericarditis can thus serve as a stressor substrate for TC. Thus, we wonder if Lee et al’s(1) finding from the second ECG can be better explained by TC or diffuse epicardial coronary vasospasm (one of the potential pathophysiological mechanisms for TC). The electrocardiographic evolution of TC is very similar to the four-stage evolution of pericarditis.(5) Furthermore, in Lee et al’s report,(1) the presence of apical hypokinesis, in addition to a mid-inferoseptal hypokinesia, may highly support our hypothesis of atypical TC superimposed on the preceding perimyocarditis. Did the authors perform a repeat echocardiography to observe any improvement in wall function? An early resolution of such hypokinesis may again be supportive of TC. Nevertheless, cardiac magnetic resonance imaging may be particularly useful for making the final diagnosis in such cases.(6,7) The telltale sign (i.e. the presence of epicardial and mid-wall late gadolinium enhancement, and an enhanced focal T2 signal representing myocardial oedema) is diagnostic of perimyocarditis.(8) On the other hand, the lack of apical late gadolinium enhancement will be more supportive of superimposed TC. Yours sincerely,

Letter by Chhabra et al Regarding Article, “Prevalence and Prognostic Significance of Abnormal P Terminal Force in Lead V1 of the Electrocardiogram in the General Population”

Eranti et al1 report an interesting correlation between an underappreciated electrocardiogram parameter, that is, P terminal force (PTF), and mortality. Indeed, PTF magnitude ≥0.04 mm·ms, if present along with an interatrial block (P-wave duration >110 ms), is considered highly specific and reasonably sensitive for diagnosing left atrial enlargement.2 The determination of PTF is restricted to lead V1, wherein lead placement error has a significant potential …