J. Sajeev

High sensitivity troponin: Does the 50% delta change alter clinical outcomes in chest pain presentations to the emergency room?

BACKGROUND The National Heart Foundation (NHF) and Cardiac Society of Australia and New Zealand (CSANZ) Acute Coronary Syndrome (ACS) guidelines recommend the use of a high sensitivity troponin assay (hsTrop) in the assessment of patients presenting with ACS. A troponin delta of 50% compared with the previously recommended 20% is advocated by the guidelines to aid in the clinical diagnosis of ACS. We sought to determine the clinical impact of the updated recommendation to use 50% troponin delta for patients presenting with chest pain to the emergency department. METHOD We retrospectively collected data for all patients >18 years presenting with chest or abdominal pain with a hsTrop test performed between January-June 2012. Patients with a STEMI, lacked serial hsTrop, were on dialysis or had trauma-related pain were excluded. RESULTS Of the 1054 eligible patients, 422 (40%) with serial hsTrop had at least one abnormal troponin (>14 ng/ml). 73 (6.9%) fell within 20-50%. Twenty-seven had clinical or ECG evidence suggestive of ACS and were referred for further cardiac investigations. Of the remainder, five patients were medically managed for ACS, 38 patients with non-cardiac chest pain had no further tests. At 1 year follow-up, of the patients that did not undergo further investigations, 6 patients represented with ACS; there was no cardiac mortality. CONCLUSION Our data showed a number of patients that would be potentially missed with the implementation of a 50% troponin. However, this loss of sensitivity was mitigated by the use of clinical acumen.

Modified positioning of a smartphone based single-lead electrocardiogram device improves detection of atrial flutter

INTRODUCTION The AliveCor Kardia Mobile (AKM) is a handheld, smartphone based cardiac rhythm monitor that records a lead-I electrocardiogram (ECG). Despite being efficacious for detection of atrial fibrillation (AF), it is unclear whether atrial flutter (AFL) may be misdiagnosed as sinus rhythm due to regular R-R intervals. We hypothesised that generating lead-II tracings through repositioning of the AKM may improve visualisation of flutter waves and clinician diagnosis of AFL compared to traditional lead-I tracings. MATERIALS AND METHODS A prospective, multi-centre, validation study was conducted comparing standard lead-I AKM positioning with lead-II in AFL. A mixed cohort of lead I tracings from patients in AF and sinus rhythm were also included. Two independent electrophysiologists (EP) analysed all ECGs blinded to the automated device diagnosis. RESULTS Fifty patients were recruited, 11 in atrial flutter, 14 in atrial fibrillation, and 25 in sinus rhythm. Lead-I AFL sensitivity was 27.3% for both EPs which individually improved to 72.7% and 54.6% in lead-II. AKM appropriately diagnosed lead-I AFL as unclassified in 18.2% of cases, compared to 54.5% in lead-II. Overall clinician agreement (AF, SR and AFL) was modest utilising AFL lead-I (EP1: κ = 0.71, EP2: κ = 0.73, p < 0.001), which improved with lead-II tracings (EP1: κ = 0.87, EP2: κ = 0.83, both p < 0.001). CONCLUSION Repositioning of the AKM device improves clinician diagnosis of atrial flutter. A lead-II tracing may be considered in high-risk patients to improve detection of atrial flutter.

Smart watches for heart rate assessment in atrial arrhythmias

BACKGROUND Despite studies demonstrating the accuracy of smart watches (SW) and wearable heart rate (HR) monitors in sinus rhythm, no data exists regarding their utility in arrhythmias. METHODS 102 hospitalized patients were evaluated at rest using continuous electrocardiogram (ECG) monitoring with concomitant SW-HR (FitBit, FB, Apple Watch, AW) for 30 min. RESULTS Across all devices, 38,616 HR values were recorded. Sinus rhythm cohort demonstrated strong agreement for both devices with a low bias (FB & AW Bias = 1 beat). In atrial arrhythmias, AW demonstrated a stronger correlation than FB (AW rs = 0.83, FB rs = 0.56, both p < 0.01) with a lower bias (Bias AW = -5 beats, FB = -18 beats). Atrial flutter demonstrated strongest agreement in both devices with a mean bias <1 beat. However, in AF, there was significant HR underestimation (Bias FB = -28 beats, AW-8 beats) with wide limits of agreement. Despite HR underestimation in AF, when SW recorded HR ≥ 100 in arrhythmias, 98% of values were within ±10-beats of ECG-HR. CONCLUSIONS SW demonstrate strong agreement for HR estimation in sinus rhythm and atrial flutter but underestimates HR in AF. Tachycardic episodes recorded at rest on a SW may be suggestive of an underlying atrial tachyarrhythmia and warrant further clinical evaluation. CLINICAL TRIAL REGISTRATION Australian New Zealand Clinical Trials Registry (www.anzctr.org.au) ACTRN: 12616001374459.

Utility of photoplethysmography for heart rate estimation among inpatients

The accuracy of photoplethysmography (PPG) for heart rate (HR) estimation in cardiac arrhythmia is unknown. PPG‐HR was evaluated in 112 hospitalised inpatients (cardiac arrhythmias (n = 60), sinus rhythm (n = 52)) using a continuous electrocardiogram monitoring as a reference standard. Strong agreement was observed in sinus rhythm HR < 100 and atrial flutter (bias 1 beat), modest agreement in sinus tachycardia (bias 24 beats) and complete heart block (bias −6 beats) and weak agreement with significant HR underestimation was seen in atrial fibrillation (bias 23 beats). Routine utilisation of PPG for HR estimation may delay early recognition of clinical deterioration in certain arrhythmias and sinus tachycardia.

Letter by Koshy et al Regarding Article, “Assessment of Remote Heart Rhythm Sampling Using the AliveCor Heart Monitor to Screen for Atrial Fibrillation: The REHEARSE-AF Study”

We read with interest the article by Halcox et al1 on the use of a smartphone-based ECG for improving atrial fibrillation (AF) detection in an intermediate-risk population. It was reassuring to see a high degree of patient compliance with transmission of ECGs obtained with a WiFi-enabled iPod (iECGs) because this is critical for successful incorporation of consumer-generated biometrics into clinical practice. The low positive predictive value of the AliveCor for the detection of AF was an interesting but unexpected observation and warrants further clarification. Among the 60 440 iECG tracings, ≈1% (600 iECGs) were categorized as AF by the automated AliveCor …

ACCURACY OF SMART WATCHES IN ARRHYTHMIAS: SMARTS STUDY

Background: Smart watches that estimate heart rate (HR) are increasingly popular and show strong correlation with HR estimated electrocardiography (ECG) among healthy controls. Although not marketed for medical use, presentations to the emergency room due to device-detected heart rate abnormalities

Takotsubo cardiomyopathy and transient global amnesia: a shared aetiology

Takotsubo cardiomyopathy (TTC) is associated with acute, reversible left ventricular (LV) dysfunction, while transient global amnesia (TGA) is a reversible disorder of the brain characterised by anterograde amnesia. We report an unusual case of TTC occurring concurrently in a patient with TGA, and propose that catecholamine surge induced cerebral venous congestion and cardiotoxicity is the shared aetiology that leads to the concurrent manifestation of these conditions. TTC and TGA are reversible disorders that can occur concurrently in a subset of patients due to a unifying aetiology, catecholamine excess, leading to pathophysiological changes within the brain and the myocardium.

Bilateral pheochromocytoma and paraganglioma: a rare cause of cardiomyopathy

A 38-year-old obese man presented with dyspnoea and signs of congestive heart failure. Transthoracic echocardiography ( Panel A ) showed severe global systolic dysfunction with a 6.7 × 2.8 cm mobile mass anchored to the apex of the left ventricle (LV) presumed to be a thrombus. Further investigations to elicit a cause of cardiomyopathy revealed markedly raised urinary metanephrines. An abdominal computed tomography (CT) scan revealed a 7.8 cm …

Stress-Induced Cardiomyopathy and Possible Link to Cerebral Executive Function: A Case Report

To the Editor: A complex and poorly understood relationship exists between cerebral and cardiac function.1 Stress produces a range of physiological responses that are relevant to cardiovascular and cerebrovascular disease. Upon stress perception, the hypothalamic-pituitary-adrenocortical (HPA) and sympatho-adrenomedullary axes are activated, increasing bioavailability of cortisol, epinephrine, and norepinephrine.2 Given the reliance of both cardiac and cerebral function on the integrity of this system, any impairment in the form of overstimulation or understimulation may manifest as cardiac and cerebrovascular pathology as illustrated in the case report below. Case report. Ms A, a 56-year-old woman with known hypertension and hypercholesterolemia, was admitted with chest pain following an argument with a family member. She had no history of ischemic heart or neurologic disease. On presentation, she was noted to be confused. Physical examination was unremarkable with no focal neurologic or cardiac abnormality identified. Further investigations revealed troponin T and creatine kinase peak concentrations of 1.15 μg/L (reference range, < 0.03 μg/L) and 614 U/L (reference range, < 180 U/L), respectively. Admission electrocardiogram (ECG) demonstrated sinus rhythm without ischemic changes (Figure 1). Computed tomography scan of the brain was unremarkable. She continued to experience amnesia over the first 12 hours after her admission; amnesia had resolved by the following day. An urgent neurology consultation was sought, and the diagnosis of transient global amnesia was made on the basis of the patient’s clinical features. Figure 1. A 12-Lead Electrocardiogram (A) At Admission, Showing Normal Sinus Rhythm, and (B) 15 Hours Later, Demonstrating Deep T-Wave Inversion Over Leads V2–V5 (anterolateral leads) Resembling Acute Coronary Ischemia Ms A was admitted to the coronary care unit; serial ECG monitoring showed biphasic and deep T-wave inversion over the anterolateral leads (see Figure 1). She underwent coronary angiography, which showed “smooth” coronary arteries and apical “ballooning” on left ventriculography consistent with takotsubo cardiomyopathy. Magnetic resonance imaging of the brain identified an incidental 6-mm left middle cerebral artery aneurysm with no associated hemorrhage or ischemia. Her final diagnoses were stress-induced (takotsubo) cardiomyopathy and transient global amnesia. Adrenergic receptors are abundant throughout the brain,3 myocardium,4 and coronary arteries.5 It is well established that catecholamine signaling through β-adrenergic receptors mediates endogenous regulation of complex central nervous system processes such as attention, arousal, learning, and memory3,6–8 as well as important cardiac functions such as chronotropy, inotropy, and lusitropy. There is general consensus that this “cerebro-cardiac” process occurs via the β-adrenoceptor–mediated cyclic-AMP (cAMP)–dependent protein kinase pathway.9–11 A growing body of evidence suggests that cortisone and epinephrine may also impair memory retrieval and therefore contribute to the mechanism of peritraumatic amnesia. de Quervain and colleagues reported that stress and infusion of cortisone impair memory retrieval in rats12 and humans.13 Sadowski et al10 demonstrated that infusion of epinephrine resulted in impairment of place and response learning. Furthermore, detrimental effects of cortisone on hippocampal function during memory retrieval have been shown to require concurrent norepinephrine-dependent activation of the basolateral part of the amygdala,14,15 which may be via an inhibitory G protein–coupled suppression of cAMP signaling.16,17 Altogether, memory formation, consolidation, and retrieval seem to be a function of β1-adrenergic receptor function, and stress impairs memory retrieval by exerting its action on the β2-adrenergic receptor. Catecholamine overstimulation has been suggested as the key pathogenetic factor in takotsubo cardiomyopathy. This cardiac syndrome is now increasingly recognized by the mental health practitioner as either a disease association18,19 or a complication of a psychiatric treatment, such as electroconvulsive therapy.20,21 Although the exact pathogenesis has not been fully elucidated, data from animal,22 imaging,23 and myocardial histologic24 studies indicate that overactive β-adrenergic signaling, in the presence of supraphysiological catecholamine concentrations, plays a significant role in mediating this phenomenon. Given the density of β-adrenergic receptors are greatest25 in the apical segments of the myocardium, Lyon and colleagues4 suggest these receptors are important in this disease phenomenon, which explains the apical propensity of transient myocardial stunning seen in takotsubo cardiomyopathy. Our case report provides a collection of cardiac and cerebral clinical findings that would support the common mechanistic link described in our review. Further understanding of this complex, dynamic relationship is required to formulate a more targeted preventive and therapeutic management strategy.