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Background: TEXTMEDS (Text Messages to Improve Medication Adherence and Secondary Prevention After Acute Coronary Syndrome) examined the effects of text message–delivered cardiac education and support on medication adherence after an acute coronary syndrome. Methods: TEXTMEDS was a single-blind, multicenter, randomized controlled trial of patients after acute coronary syndrome. The control group received usual care (secondary prevention as determined by the treating clinician); the intervention group also received multiple motivational and supportive weekly text messages on medications and healthy lifestyle with the opportunity for 2-way communication (text or telephone). The primary end point of self-reported medication adherence was the percentage of patients who were adherent, defined as >80% adherence to each of up to 5 indicated cardioprotective medications, at both 6 and 12 months. Results: A total of 1424 patients (mean age, 58 years [SD, 11]; 79% male) were randomized from 18 Australian public teaching hospitals. There was no significant difference in the primary end point of self-reported medication adherence between the intervention and control groups (relative risk, 0.93 [95% CI, 0.84–1.03]; P =0.15). There was no difference between intervention and control groups at 12 months in adherence to individual medications (aspirin, 96% vs 96%; β-blocker, 84% vs 84%; angiotensin-converting enzyme inhibitor/angiotensin receptor blocker, 77% vs 80%; statin, 95% vs 95%; second antiplatelet, 84% vs 84% [all P >0.05]), systolic blood pressure (130 vs 129 mm Hg; P =0.26), low-density lipoprotein cholesterol (2.0 vs 1.9 mmol/L; P =0.34), smoking ( P =0.59), or exercising regularly (71% vs 68%; P =0.52). There were small differences in lifestyle risk factors in favor of intervention on body mass index 2 (21% vs 18%; P =0.01), eating ≥5 servings per day of vegetables (9% vs 5%; P =0.03), and eating ≥2 servings per day of fruit (44% vs 39%; P =0.01). Conclusions: A text message–based program had no effect on medical adherence but small effects on lifestyle risk factors. Registration: URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=364448 ; Unique identifier: ANZCTR ACTRN12613000793718.

Background: Treating known risk factors for coronary artery disease (CAD) has substantially reduced CAD morbidity and mortality. However, a significant burden of CAD remains unexplained. Immunoglobulin E sensitization to mammalian oligosaccharide galactose-α-1,3-galactose (α-Gal) was recently associated with CAD in a small observational study. We sought to confirm that α-Gal sensitization is associated with CAD burden, in particular noncalcified plaque. Additionally, we sort to assess whether that α-Gal sensitization is associated with ST-segment–elevated myocardial infarction (STEMI) Methods: We performed a cross-sectional analysis of participants enrolled in the BioHEART cohort study. We measured α-Gal specific-immunoglobulin E antibodies in serum of 1056 patients referred for CT coronary angiography for suspected CAD and 100 selected patients presenting with STEMI, enriched for patients without standard modifiable risk factors. CT coronary angiograms were assessed using coronary artery calcium scores and segmental plaque scores. Results: α-Gal sensitization was associated with presence of noncalcified plaque (odds ratio, 1.62 [95% CI, 1.04–2.53], P =0.03) and obstructive CAD (odds ratio, 2.05 [95% CI, 1.29-3.25], P =0.002), independent of age, sex, and traditional risk factors. The α-Gal sensitization rate was 12.8-fold higher in patients with STEMI compared with matched healthy controls and 2.2-fold higher in the patients with STEMI compared with matched stable CAD patients (17% versus 1.3%, P =0.01 and 20% versus 9%, P =0.03, respectively). Conclusions: α-Gal sensitization is independently associated with noncalcified plaque burden and obstructive CAD and occurs at higher frequency in patients with STEMI than those with stable or no CAD. These findings may have implications for individuals exposed to ticks, as well as public health policy. Registration: URL: https://www.anzctr.org.au ; Unique identifier: ACTRN12618001322224.

Background The pathophysiological mechanism behind adverse outcomes associated with ischemia‐inducing epicardial coronary stenoses and microcirculatory dysfunction remains unclear. Wall shear stress (WSS) plays an important role in atherosclerotic plaque progression and vulnerability. We aimed to evaluate the relationship between WSS, functionally significant epicardial coronary stenoses, and microcirculatory dysfunction. Methods and Results Patients undergoing invasive coronary physiology testing were included. Fractional flow reserve, instantaneous wave‐free ratio, and the index of microcirculatory resistance were measured. Quantitative coronary angiography was used to obtain the lesion percentage diameter stenosis. Computational fluid dynamics analysis was performed to calculate WSS parameters. Multiple regression analysis was performed to calculate the standardized regression coefficient (β) for the coronary physiology indices. A total of 107 vessels from 88 patients were included. Fractional flow reserve independently predicted the total area of low WSS (β=−0.44; 95% CI, −0.62 to −0.25; P P P P Conclusions Fractional flow reserve and instantaneous wave‐free ratio independently predicted the total burden of low WSS and maximum lesion WSS in coronary arteries. No relationship was found between microcirculatory dysfunction and WSS.

Introduction: Cardiac complications of COVID-19 include acute cardiac injury, myopericarditis, cardiomyopathy and arrhythmias. This study aimed to describe the incidence of cardiac complications in patients admitted to hospital with COVID-19 in Australia. Methods: AUS-COVID is a multicentre observational cohort study across 21 Australian hospitals including all index hospitalisations with laboratory-proven COVID-19 in patients aged 18 years or older. All consecutive patients entered in the AUS-COVID Registry by 28 th January 2021 were included in the present study. Results: Six hundred and forty-four hospitalised patients (62.5 ± 20.1 years old, 51.1% male) with COVID-19 were enrolled in the study. Overall in-hospital mortality was 14.3%. Twenty (3.6%) patients developed new atrial fibrillation or flutter during admission and 9 (1.6%) patients were diagnosed with new heart failure or cardiomyopathy. Three (0.5%) patients developed high grade atrioventricular (AV) block. Two (0.3%) patients were clinically diagnosed with pericarditis or myopericarditis. Among the 295 (45.8%) patients with at least one troponin measurement, 99 (33.6%) had a peak troponin above the upper limit of normal (ULN). In-hospital mortality was higher in patients with raised troponin (32.3% vs 6.1%, p Conclusions: Among patients with COVID-19 requiring hospitalisation in Australia, troponin elevation was common but clinical cardiac sequelae were uncommon. The incidence of atrial arrhythmias and troponin elevation was greatest in patients 65 years and older. Trial registration: AUS-COVID. ACTRN12620000486921. http://www.anzctr.org.au/

Introduction: To assess whether hypertension is an independent risk factor for mortality amongst patients hospitalised with COVID-19 and to evaluate the impact of angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) on mortality in patients with a background of hypertension. Methods: This observational cohort study included all consecutive index hospitalisations with laboratory proven COVID-19 aged 18 years or older across 21 Australian hospitals entered in the AUS-COVID Registry by 22nd January 2021. Patients were excluded if their past medical or medication history was not available or if they were transferred to another hospital in which case mortality outcomes were not available. Registry data were analysed for in-hospital mortality in patients with comorbidities including hypertension, and baseline treatment with ACE inhibitors or ARBs. Results: 546 consecutive patients (62.9±19.8 years old, 51.8% male) hospitalised with COVID-19 were enrolled. In the multivariable model, significant predictors of mortality were age (aOR 1.09, 95% CI 1.07-1.12, p Conclusions: In patients hospitalised with COVID-19, pre-existing hypertension was the most prevalent comorbidity but was not independently associated with mortality. Similarly, the baseline use of ACE inhibitors or ARBs had no independent association with in-hospital mortality.

Percutaneous coronary intervention is the most common mode of revascularization and is increasingly undertaken in high-risk subsets, including the elderly. The presence of coronary artery calcification is increasingly observed and significantly limits technical success. The mechanisms for this are multi-factorial, including increased arterial wall stiffness and impaired delivery of devices, leading to suboptimal stent delivery, deployment, and expansion which are harbingers for increased risk of in-stent restenosis and stent thrombosis. Although conventional balloon pretreatment techniques aim to mitigate this risk by modifying the lesion before stent placement, many lesions remain resistant to conventional strategies, due to the severity of calcification. There have been several substantial technological advancements in calcium modification methods in recent years, which have allowed improved procedural success with low periprocedural complication rates. This review will summarize the current adjunctive modification technologies that can be employed to improve technical outcomes in percutaneous coronary intervention in calcific disease and the evidence supporting these tools.

Opposing Viewpoint, see p 1571 In most advanced healthcare systems, primary percutaneous coronary intervention (PPCI) has replaced thrombolysis as the optimal therapy for patients presenting with ST-segment–elevation acute myocardial infarction (STEMI). The frequent discovery of nonculprit vessel lesions during this index revascularization has fueled enthusiasm among interventional cardiologists to implant additional stents at the time of PPCI. The potential for cost saving by preventing an additional second procedure, reductions in inpatient stay, and even mortality benefits from immediate complete revascularization have been hypothesized. Determining whether this approach is a rational extension of the index emergency revascularization procedure or a costly and potentially hazardous extrapolation of the benefits of coronary stents has sparked considerable debate. Disease in the nonculprit vessel in patients with STEMI is common; it is present in up to 60% of patients and, predictably, its presence is associated with worse outcomes.1 A pooled meta-analysis of 40 280 patients published in 2011 suggested that staged percutaneous coronary intervention (PCI) of nonculprit lesions yielded superior short- and long-term outcomes in comparison with culprit lesion–only treatment, whereas multivessel PCI resulted in worse outcomes to culprit-only PCI or staged PCI.1 Because this retrospective analysis is subject to confounding (multivessel PCI performed preferentially for cardiogenic shock), 3 …

Autophagy is a cellular process by which mammalian cells degrade and recycle damaged organelles and proteins. Remote ischemic preconditioning (RIPC) protects the myocardium from ischemia-reperfusion (I/R) injury and is thought to involve upregulation of autophagy. In this study we aim to ascertain the role of autophagy in RIPC induced cardioprotection. Sprague Dawley rats were subjected to transient blockade of left anterior descending coronary artery to simulate I/R injury, with or without prior RIPC at the hind limb. RIPC prior I/R decreased myocardial infarct size (51.5 ± 3.5% vs. 30.2 ± 5.16%; n=7, p

Many forms of cardiovascular disease (CVD) demonstrate heritability and thus a genetic contribution is likely. This is most evident when considering the "simple" Mendelian traits such as hypertrophic cardiomyopathy. However, family history also influences our assessment of patients with complex traits such as coronary artery disease, hypertension, and common forms of hypercholesterolemia, as observed in clinical practice. Recent research has led to advances in our understanding of the genetic basis of both the simple and complex forms of CVD. This review presents the current state of knowledge regarding major gene disorders, as well as more common, complex forms of CVD such as coronary artery disease. It discusses the fundamental approaches being used to identify the genetic basis of the various disease states, as well as the practical implications of the discoveries to clinicians. It also focuses on our need to assess the extent by which genetic analysis can alter our calculation of an individual's risk of disease, and our ability to successfully target treatment that will modify this process.

Vascular injury initiates a cascade of phenotype-altering molecular events. Transcription factor function in this process, particularly that of negative regulators, is poorly understood. We demonstrate here that the forced expression of the injury-inducible GLI-Krüppel zinc finger protein Yin Yang-1 (YY1) inhibits neointima formation in human, rabbit and rat blood vessels. YY1 inhibits p21 WAF1/Cip1 transcription, prevents assembly of a p21 WAF1/Cip1 -cdk4-cyclin D1 complex, and blocks downstream pRb Ser249/Thr252 phosphorylation and expression of PCNA and TK-1. Conversely, suppression of endogenous YY1 elevates levels of p21 WAF1/Cip1 , PCNA, pRb Ser249/Thr252 and TK-1, and increases intimal thickening. YY1 binds Sp1 and prevents its occupancy of a distinct element in the p21 WAF1/Cip1 promoter without YY1 itself binding the promoter. Additionally, YY1 induces ubiquitination and proteasome-dependent degradation of p53, decreasing p53 immunoreactivity in the artery wall. These findings define a new role for YY1 as both an inducer of p53 instability in smooth muscle cells, and an indirect repressor of p21 WAF1/Cip1 transcription, p21 WAF1/Cip1 -cdk4-cyclin D1 assembly and intimal thickening.

Introduction: Quantification of myocardial “area-at-risk” (AAR) and infarct (MI) zone is critical for assessing novel therapies targeting myocardial ischemia-reperfusion (IR) injury. The current standard method involves perfusion with Evan’s Blue (EB), staining with TTC and manual slicing and analysis. We have developed an MRI method for quantifying MI and AAR in whole hearts which provides superior 3D resolution to the standard approach. Methods: Rats were given an IR injury, recovered for 24 hours then infused with Gd-DTPA via the tail vein. The coronary artery was then religated, and a solution containing both iron oxide microparticles and EB was infused. For comparison, hearts were then harvested and transversally sectioned for TTC staining. Some hearts were kept intact for MRI only analysis. Ex-vivo MRI T2* and T1 images were acquired on a 9.4T magnet. The AAR (red) was quantified by comparing the T2* signal loss in perfused regions (blue) and high T1-signal in infarcted zones (white) from Gd-DTPA retention. Results: MRI and EB/TTC measures on the same slice for both AAR and MI were highly correlated (r=0.92-0.94;p Conclusion: This novel MRI technique allows precise assessment of infarct and AAR zones and is highly suited to automation of both analysis and acquisition. This method could remove the need for tissue slicing, and via a centralised MRI facility, could permit 3D digital analysis of hearts at high anatomical resolution, accessible for all laboratories already performing IR experiments.

Background Egr‐1 is implicated in the pathogenesis of myocardial ischemia–reperfusion injury. The aim of this study was to ascertain the effectiveness of intracoronary delivery of DNA zyme targeting the transcription factor Egr‐1 at reperfusion following experimental myocardial ischemia. Methods and Results Functional DNA zyme targeting Egr‐1 or a size‐matched scrambled control were delivered via the intracoronary route immediately on reperfusion after 60 minutes' balloon occlusion of the left anterior descending coronary artery in a pig model of myocardial I/R injury (n=7 per treatment group). Heart function and extent of myocardial infarction were determined following intervention by echocardiography and cardiac magnetic resonance imaging, respectively. Hearts were removed and examined for molecular and histological markers of inflammation and apoptosis. Administration of functional DNA zyme led to an overall decrease in the expression of inflammatory markers including intracellular adhesion molecule‐1, tissue factor, and complement 3, with associated decreases in the extent of neutrophil infiltration, oxidative damage, and subsequent apoptosis within the infarct border zone. Functional significance was indicated by an increase in salvaged left ventricular myocardium ( P =0.012), ejection fraction ( P =0.002), and fractional area change ( P =0.039) in the functional DNA zyme–treated group compared with the control. Conclusions Egr‐1 silencing through intracoronary delivery of a targeting DNA zyme at the time of reperfusion following acute myocardial ischemia decreases myocardial inflammation and apoptosis leading to improved cardiac function.

To the Editor: Garg and colleagues1 demonstrate no association between migraines and patent foramen ovale (PFO) in their recent case control study. Although their observations are interesting, the implications of this, another small case control …

To the Editor: We have carefully read the interesting article of Finn et al1 that focused on the pivotal issue of late stent thrombosis in drug-eluting stents. From a registry of 81 human autopsies comprising 109 coronary lesions treated with drug-eluting stents, the authors identified 28 lesions with thrombus formation. They concluded that the most powerful predictor of stent thrombosis is the ratio of uncovered to total struts per section. Some points, in our opinion, deserve further clarification. First, the main inclusion criterion …

An 82-year-old man presented with an acute anterior myocardial infarction and was treated with intravenous reteplase with successful reperfusion. Forty-eight hours later, however, he developed further chest pain and ST-segment elevation. He was referred for salvage percutaneous coronary intervention. The left anterior descending artery was completely occluded proximally (Figure, A) with no detectable collateral flow, and the remainder of the coronary circulation showed diffuse nonsignificant disease. The left anterior descending artery was engaged with a JL4 guide catheter and wired with a Whisper J wire. The lesion was predilated with …