Hypertrophic cardiomyopathy is a complex genetic cardiovascular disorder with substantial variability in phenotypic expression and natural progression. Recent research demonstrates the incremental utility of cardiac magnetic resonance in the diagnosis, therapeutic planning, and prognostication of this disease. The increasing incorporation of multimodality imaging of hypertrophic cardiomyopathy in clinical practice will continue to improve our understanding of the subtle morphologic differences and their prognostic implications.

The reservoir, conduit, and contractile functions of the left atrium are integral to overall cardiac performance. Recent advances in cardiac imaging offer the accurate assessment of LA phasic functions and structure, using techniques such as 3-dimensional echocardiography, color tissue Doppler imaging, and speckle tracking, as well as cardiac computed tomography and magnetic resonance imaging. These new developments are particularly important in view of the increasing use of intervention involving the left atrium. This review article highlights and contrasts the imaging of the size, mechanics, and structure of the left atrium using multiple modalities. The authors discuss recent studies on the clinical applications of the various techniques in disease conditions.

Our systematic review of more than 3000 HCM patients suggests an association of abnormal LV-GLS with adverse composite cardiac outcomes and ventricular arrhythmias.

AF is common in haemodialysis patients. The incidence of major haemorrhage was over three times that of cerebrovascular accidents. Guideline recommendations for anticoagulation in AF in the general population may not be appropriate for the haemodialysis population.

Background: Efforts to safely reduce length of stay for emergency department patients with symptoms suggestive of acute coronary syndrome (ACS) have had mixed success. Few system-wide efforts affecting multiple hospital emergency departments have ever been evaluated. We evaluated the effectiveness of a nationwide implementation of clinical pathways for potential ACS in disparate hospitals. Methods: This was a multicenter pragmatic stepped-wedge before-and-after trial in 7 New Zealand acute care hospitals with 31 332 patients investigated for suspected ACS with serial troponin measurements. The implementation was a clinical pathway for the assessment of patients with suspected ACS that included a clinical pathway document in paper or electronic format, structured risk stratification, specified time points for electrocardiographic and serial troponin testing within 3 hours of arrival, and directions for combining risk stratification and electrocardiographic and troponin testing in an accelerated diagnostic protocol. Implementation was monitored for >4 months and compared with usual care over the preceding 6 months. The main outcome measure was the odds of discharge within 6 hours of presentation Results: There were 11 529 participants in the preimplementation phase (range, 284–3465) and 19 803 in the postimplementation phase (range, 395–5039). Overall, the mean 6-hour discharge rate increased from 8.3% (range, 2.7%–37.7%) to 18.4% (6.8%–43.8%). The odds of being discharged within 6 hours increased after clinical pathway implementation. The odds ratio was 2.4 (95% confidence interval, 2.3–2.6). In patients without ACS, the median length of hospital stays decreased by 2.9 hours (95% confidence interval, 2.4–3.4). For patients discharged within 6 hours, there was no change in 30-day major adverse cardiac event rates (0.52% versus 0.44%; P =0.96). In these patients, no adverse event occurred when clinical pathways were correctly followed. Conclusions: Implementation of clinical pathways for suspected ACS reduced the length of stay and increased the proportions of patients safely discharged within 6 hours. Clinical Trial Registration: URL: https://www.anzctr.org.au/ (Australian and New Zealand Clinical Trials Registry). Unique identifier: ACTRN12617000381381.

ObjectiveTakotsubo syndrome (TS) mimics acute coronary syndrome (ACS) but has a distinct pathophysiology. While in-hospital adverse outcomes appear similar to those presenting with an ACS, data on longer term postdischarge risk are conflicting. This study sought to assess the long-term prognosis of patients discharged alive after TS.MethodsThe clinical profile and in-hospital and long-term outcomes were prospectively assessed in consecutive patients with TS. Survival in patients with TS was compared with two representative age-matched and gender-matched comparison cohorts: a hospitalised ACS cohort and a community cohort without known cardiovascular disease (CVD).ResultsTwo hundred and-twenty-five patients with TS (216 women, mean age 63.7±11.8 years) were included. In-hospital mortality was 1.8% and 1.9% for patients with TS and ACS, respectively. Of the 219 patients with TS with postdischarge follow-up, at a mean follow-up of 4.8±3.2 years, there were 19 (8.3%) deaths, 18 of which were from non-cardiac causes. When compared with the cohort without prior CVD, postdischarge patients with TS were at increased mortality risk (HR 2.00, 95% CI 1.26 to 3.17, p=0.003), but mortality in postdischarge patients with ACS was over threefold higher (HR 3.43, 95% CI 2.97 to 3.96, p<0.0001).ConclusionsIn-hospital mortality for patients diagnosed with TS and ACS was similar. However, while postdischarge survivors of TS had a long-term survival which was poorer than for a community-based cohort without known CVD, their survival was better than for postdischarge survivors of an ACS event. Late deaths in patients with TS were almost all from non-cardiac causes.

Electrocardiogram (ECG)-based detection of left ventricular systolic dysfunction (LVSD) has poor specificity and positive predictive value, even when including major ECG abnormalities, such as left bundle branch block (LBBB) within the criteria for diagnosis. Although machine-read ECG algorithms do not provide information on LVSD, advanced ECG (A-ECG), using multiparameter scores, has superior diagnostic utility to strictly conventional ECG for identifying various cardiac pathologies, including LVSD. Methods: We evaluated the diagnostic utility of A-ECG in a case-control study of 40 patients with LVSD (LV ejection fraction < 50% by echocardiography), due to non-ischemic cardiomyopathy (NICM), and 39 other patients without LVSD. Diagnostic sensitivity and specificity for LVSD were determined after applying a previously validated probabilistic A-ECG score for LVSD to stored standard (10 s) clinical 12L ECGs. In 25 of the NICM patients who had serial ECGs and echocardiograms, changes in the A-ECG score versus in echocardiographic LV ejection fraction were also studied to determine the level of agreement between the two tests. Results: Analyses by A-ECG had a sensitivity of 95% for LVSD (93% if excluding N = 11 patients with LBBB) and specificity of 95%. In the 29 NICM patients without LBBB who had serial ECGs, sensitivity improved to 97% when all ECGs were considered. By comparison, human readers in a busy clinical environment had a sensitivity of 90% and specificity of 63%. A-ECG score trajectories demonstrated improvement, deterioration or no change in LVSD, which agreed with echocardiography, in 76% of cases (n = 25). Conclusion: A-ECG scoring detects LVSD due to NICM with high sensitivity and specificity. Serial A-ECG score trajectories also represent a method for inexpensively demonstrating changes in LVSD. A-ECG scoring may be of particular value in areas where echocardiography is unavailable, or as a gatekeeper for echocardiography.

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