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Background and aims: Current ESC guidelines on the management of patients after acute myocardial infarction only include the evaluation of left ventricular (LV) function by assessment of the ejection fraction in addition to clinical risk scores to estimate the patient's prognosis. We aimed to determine, whether comprehensive evaluation of cardiac function using LV and right ventricular (RV) global longitudinal strain (GLS) and left atrial (LA) reservoir strain improves the prediction of survival in patients with acute myocardial infarction.

Methods: In patients with non-ST segment elevation or ST segment elevation myocardial infarction receiving echocardiography within 1 year after revascularisation, LV-GLS, RV-GLS and LA reservoir strain were quantified. In multivariable Cox regression analysis, HRs and 95% CIs were calculated per 1 SD increase in strain measure, adjusting for age, sex, systolic blood pressure, low-density lipoprotein cholesterol, smoking, diabetes and family history of premature coronary artery disease.

Results: During a median follow-up of 1.5 (0.5-4.2) years, 157 (11.1%) out of 1409 patients (64.4±13.5 years, 24.7% female) died. LV-GLS (1.68 (1.37-2.06), p<0.001), RV-GLS (1.39 (1.16-1.67), p<0.001) and LA reservoir strain (0.57 (0.47-0.69), p<0.001) were associated with mortality. Adding LV ejection fraction, tricuspid annular plane systolic excursion (TAPSE) or LA volume index to these models did not alter the association of strain measures of the LV (1.41 (1.06-1.89), p=0.02), RV (1.48 (1.03-2.13), p=0.04) or LA (0.61 (0.49-0.76), p<0.001). In receiver operating characteristics, combining the three strain measures improved the prediction of mortality above risk factors (AUC: 0.67 (0.63-0.71) to 0.75 (0.70-0.80)), while further addition of LV ejection fraction, TAPSE and LA volume index did not (0.75 (0.70-0.81)).

Conclusion: The comprehensive evaluation of contractility of various cardiac chambers via transthoracic echocardiography using myocardial strain analysis, when routinely performed after acute myocardial infarction, may help to detect patients at increased mortality risk.

Background: Fabry disease (FD) causes multiorgan sphingolipid accumulation, with cardiac involvement responsible for the largest burden of morbidity and mortality. Exercise intolerance in FD is prevalent, yet the mechanisms of this are poorly understood. The aim of this study was to assess exercise intolerance in FD and identify whether this correlates with the phase of cardiomyopathy.

Methods: This was a retrospective observational study of adults with FD undergoing cardiopulmonary exercise testing (CPEX) between September 2011 and September 2023 at a national referral centre in the UK. The primary outcome measure was peak oxygen uptake (V̇O_2peak), with forced expiratory volume in 1 s (FEV₁) used to quantify respiratory impairment. Age-normalised/sex-normalised values were additionally calculated, based on published normal ranges for subgroups of age and sex. The cardiomyopathy phase was classified on a 4-point scale by two FD experts using contemporaneous imaging and biochemistry results.

Results: CPEX was completed by 42 patients, with a median age of 54 years and of whom 62% were male. Patients were approximately equally distributed across the four cardiomyopathy phases. At phase I, the mean (±SD) V̇O_2peak was 28.7±7.7 mL/kg/min, which represented a significant underperformance of 23%, relative to age-normalised and sex-normalised values (expected mean: 37.3±3.2 mL/kg/min, p=0.006). V̇O_2peak declined significantly across the cardiomyopathy phases (p=0.010), reaching a mean of 21.2±6.1 mL/kg/min at phase IV. Normalised FEV₁ was not found to show a corresponding significant change with cardiomyopathy phase (p=0.683). Impaired left atrial global longitudinal strain as well as biochemical markers of inflammation were associated with impaired V̇O_2peak.

Conclusions: This study identifies significantly impaired aerobic capacity in FD, even in those without phenotypic cardiomyopathy. No corresponding changes in respiratory impairment were observed, suggesting that exercise intolerance may be due to early cardiac sphingolipid accumulation and subsequent atrial and ventricular dysfunction, which increases as cardiomyopathy progresses. As such, peak V̇O_2peak holds promise as a therapeutic marker of response to FD-specific therapy.

Background: Patients with Takotsubo syndrome (TTS) who develop cardiogenic shock may present with left ventricular outflow tract obstruction (LVOTO). The prognosis and treatment of this population have not been defined in previous studies. The aim of this study is to describe the clinical presentation, management, evolution and prognosis of a subgroup of patients with TTS and cardiogenic shock according to whether they present with LVOTO or not.

Methods: We analysed patients with TTS recruited from 2003 to 2022 in a multicentre registry. Patients were selected if they presented cardiogenic shock during their admission. This analysis was compared according to the presence or absence of LVOTO.

Results: 322 patients were included, 58 (18%) of whom had LVOTO. The majority were treated with vasoactive and inotropic therapy (VIT) and its use was strongly associated with having LVOTO (77.6% vs 57.6%, p<0.001). Only five (3.3%) patients without LVOTO and two (4.4%) in the LVOTO group treated with VIT developed or worsened the obstruction. Furthermore, patients with LVOTO presented higher in-hospital complications including ventricular arrhythmias (15.5% vs 8.7%, p=0.017), major bleeding (13.8% vs 6.1%, p=0.042) and acute kidney failure (48.3% vs 28.4%, p=0.003). However, at both 90 days and 5 years, the cumulative incidence of all-cause death was not significantly different between the patients with and without LVOTO (HR 1.20, 95% CI 0.60 to 2.40 for 90 days, and HR 1.69, 95% CI 0.89 to 3.21 for 5 years).

Conclusions: LVOTO is not uncommon in patients with TTS and cardiogenic shock. It is associated with a more aggressive in-hospital course and our data is unable to rule out an association between the presence of LVOTO and long-term prognosis of patients with TTS. The development or worsening of LVOTO directly related to inotropic or vasoactive support was low.

Background: Studies predating widespread COVID-19 vaccination identified patients with congenital heart disease (CHD) as a group at increased risk of severe outcomes from COVID-19. Here we evaluate the impact of vaccination on COVID-19 outcomes among patients with CHD.

Methods: We conducted a case-control study using linked English electronic health records (n=3 18 135). Patients with CHD were matched with controls by age, sex, ethnicity and GP practice. The 'prevaccination' cohort comprised unvaccinated patients with CHD and matched controls with first-recorded SARS-CoV-2 infection between 1 March and 8 December 2020 (7805 cases, 27 620 controls). The 'post-vaccination' cohort comprised vaccinated patients with CHD and matched controls with first-recorded SARS-CoV-2 infection between 1 March 2021 and 1 April 2022, at least 14 days after vaccination (57 550 cases, 225 160 controls). Odds of severe COVID-19 outcomes were compared using conditional logistic regression. We also compared the rate at which vaccine efficacy diminished, and the incidence of vaccine-associated complications.

Results: Compared with the prevaccination cohort, postvaccination patients with CHD exhibited markedly reduced rates of COVID-19-related hospitalisation (0.5% vs 15.8%) and mortality rates (0.5% vs 4.6%). Compared with vaccinated controls, vaccinated patients with CHD remained at increased risk of hospitalisation (0.5% vs 0.2%, adjusted OR 2.24 (1.88-2.65); p<0.001) and death (0.5% vs 0.3%, adjusted OR 1.81 (1.54-2.13); p<0.001). There was no evidence that vaccine efficacy declined faster in patients with CHD, or that patients with CHD experienced a larger increase in incidence of myocarditis, pericarditis or thrombotic events.

Conclusion: We observed a lower absolute risk of hospitalisation and death from COVID-19 in CHD patients after vaccination. However, in vaccinated CHD patients, an elevated risk of severe outcomes persists compared with vaccinated people without CHD. These results emphasise the importance of vaccination in the CHD population, and of vigilance among care providers dealing with COVID-19 infection in CHD patients, even if fully vaccinated.

Background: Long-term outcome of contemporary stress echocardiography has not been systematically assessed.

Objective: To evaluate the association between results of stress echocardiography and patients' outcomes with suspected coronary artery disease using randomised controlled trials.

Methods: Multiple electronic databases were searched for studies evaluating long-term outcome (>12 months) of stress echocardiography in patients suspected of coronary artery disease since year 2000. A common-effect model was used to derive pooled estimates. The primary outcome was a composite of all-cause mortality or cardiovascular death and non-fatal myocardial infarction, depending on the definition applied in individual trials, termed as major adverse cardiovascular event (MACE). Secondary outcome was all-cause mortality. Positive stress echocardiography result was defined as inducible ischaemia in at least one of the 17 left ventricular segments and negative stress echocardiography with no inducible ischaemia.

Results: Among a total of six trials, 16 581 subjects underwent either pharmacological or treadmill stress echocardiography, a median follow-up of 31 months (range 21-101). The annual event rate was 1.76% for the composite MACE and 1.35% for all-cause mortality. Compared with negative stress echocardiography, positive stress echocardiography was associated with an increased risk of the MACE and all-cause mortality with an annual event rate of 1.99% vs 1.54% (OR 2.04, 95% CI 1.79 to 2.33) and 1.68% vs 1.02% (OR 2.06, 95% CI 1.80 to 2.35), respectively.

Conclusion: Positive stress echocardiography results were associated with poorer long-term MACE and all-cause mortality. Stress echocardiography results may provide a useful long-term guidance in intensifying preventative treatment in patients with suspected coronary artery disease.

Prospero registration number: CRD42023416766.

Background: Patients with psychiatric disorders have increased all-cause mortality compared with the general population. Previous research has shown that there is a fourfold increased risk of sudden cardiac death (SCD) among the young.

Objective: To investigate the incidence of SCD in patients with psychiatric disorders aged 18-90 years in the Danish population by systematically reviewing all deaths in 1 year.

Methods: We examined all deaths in Denmark among residents aged 18-90 years in 2010 by reviewing death certificates and autopsy reports. All deaths were categorised as non-SCD or SCD based on the available information. Psychiatric disorder was defined according to International Classification of Diseases, 10th revision criteria or by redemption of a prescription for psychotropic medication within 1 year.

Results: Of 4.3 million residents in 2010, we observed 45 703 deaths, of which 6002 were due to SCD. Overall, the incidence rate ratio of SCD was 1.79-6.45 times higher among patients with psychiatric disorders than in the general population and was age dependent (p<0.001 across all age groups). When adjusting for age, sex and comorbidities, psychiatric disorders were independently associated with SCD, with a HR of 2.31 (2.19 to 2.43, p<0.001), and HR was highest among patients with schizophrenic disorders, with a HR of 4.51 (3.95 to 5.16, p <0.001). Furthermore, 18-year-old patients with a psychiatric disorder had an expected 10-year excess loss of life. Patients aged 18-40 with a psychiatric disorder had 13% of excess life years lost caused by SCD.

Conclusion: In this study, the rate of SCD in patients with psychiatric disorders is higher across all age groups than in the general population. Having a psychiatric disorder is independently associated with SCD. Patients with schizophrenic disease had the highest rates of SCD. Life expectancy for an 18-year old with a psychiatric disorder is estimated to be 10 years shorter in comparison with those without this disorder.