This study investigated the relation between psychotropic medication use and adverse cardiovascular (CV) events in women with symptoms of myocardial ischaemia undergoing coronary angiography.
Women enrolled in the Women’s Ischemia Syndrome Evaluation (WISE) were classified into one of four groups according to their reported antidepressant and anxiolytic medication usage at study intake: (1) no medication (n = 352); (2) anxiolytics only (n = 67); (3) antidepressants only (n = 58); and (4) combined antidepressant and anxiolytics (n = 39). Participants were followed prospectively for the development of adverse CV events (for example, hospitalisations for non-fatal myocardial infarction, stroke, congestive heart failure and unstable angina) or all-cause mortality over a median of 5.9 years.
Use of antidepressant medication was associated with subsequent CV events (HR 2.16, 95% CI 1.21 to 3.93) and death (HR 2.15, 95% CI 1.16 to 3.98) but baseline anxiolytic use alone did not predict subsequent CV events and death. In a final regression model that included demographics, depression and anxiety symptoms, and risk factors for cardiovascular disease, women in the combined medication group (that is, antidepressants and anxiolytics) had higher risk for CV events (HR 3.98, CI 1.74 to 9.10, p = 0.001 and all-cause mortality (HR 4.70, CI 1.7 to 2.97, p = 0.003) compared to those using neither medication. Kaplan-Meier survival curves indicated that there was a significant difference in mortality among the four medication groups (p = 0.001).
These data suggest that factors related to psychotropic medication such as depression refractory to treatment, or medication use itself, are associated with adverse CV events in women with suspected myocardial ischaemia.
To evaluate the vascular response at 9 months after zotarolimus-eluting stent (ZES; Endeavor) implantation using optical coherence tomography (OCT). These findings were compared with those after implantation of a sirolimus-eluting stent (SES; Cypher Select).
Cross-sectional observational study with prospective OCT registry.
Nine months after ZES or SES implantation.
A total of 68 patients (32 ZES and 36 SES) underwent OCT at 9 months after stent implantation. The neointima hyperplasia (NIH) thickness inside each strut and percentage of NIH area at every 1 mm cross section were measured.
The degree of neointimal coverage and the prevalence of malapposition at 9 months after ZES and SES implantation using OCT.
The mean (SD) NIH thickness (251.2 (110.0) µm vs 85.5 (53.3) µm, p<0.001) and percentage of NIH area (27.9 (9.1)% vs 11.2 (7.1)%, p<0.001) were significantly greater in ZES than in SES. The prevalence of uncovered strut as well as malapposed strut was significantly lower in ZES than in SES (0.3% vs 12.3%, p<0.001 and 0.08% vs 2.6%, p<0.001). Thrombus was not observed in ZES (0.0% in ZES vs 27.8% in SES, p = 0.001).
Neointimal coverage in ZES was almost complete and malapposition was very rare at 9-months’ follow-up.
To observe and characterise vessel injury after stenting using optical coherence tomography (OCT), to propose a systematic OCT classification for periprocedural vessel trauma, to evaluate its frequency in stable versus unstable patients and to assess its clinical impact during the hospitalisation period.
Stenting causes vessel injury.
All consecutive patients in whom OCT was performed after stent implantation were included in the study. Qualitative and quantitative assessment of tissue prolapse, intra-stent dissection and edge dissection were performed.
Seventy-three patients (80 vessels) were analysed. Tissue prolapse within the stented segment was visible in 78/80 vessels (97.5%). Median number of tissue prolapse sites was 8 (IQR 4–19), mean (SD) area 1.04 (0.9) mm2. Intra-stent dissection flaps were visible in 69/80 vessels (86.3%) (median number 3 (IQR 1.25–6), maximum flap length 450 (220) µm). Fifty-five out of 80 vessels (68.8%) showed dissection cavities (median number 2 (IQR 0–4.75), maximum depth 340 (170) µm). Edge dissection was visible in 20 vessels (mean (SD) length flap 744 (439) µm). The frequency of tissue prolapse or intra-stent dissection was similar in stable and unstable patients (95.6% vs 100%, p = 0.5 for tissue prolapse; 91.1% vs 82.9%, p = 0.3 for intra-stent dissection). There were no events during the hospitalisation period.
OCT allows a detailed visualisation of vessel injury after stent implantation and enables a systematic classification and quantification in vivo. In this study, frequency of tissue prolapse or intra-stent dissections after stenting was high, irrespective of the clinical presentation of the patients, and was not associated with clinical events during hospitalisation.
Aldosterone has a key role in the pathophysiology of heart failure. In around 50% of such patients, aldosterone "escapes" from inhibition by drugs that interrupt the renin-angiotensin axis; such patients have a worse clinical outcome. Insulin resistance is a risk factor in heart failure and cardiovascular disease. The relation between aldosterone status and insulin sensitivity was investigated in a cohort of heart failure patients.
302 patients with New York Heart Association (NYHA) class II-IV heart failure on conventional therapy were randomised in the ALiskiren Observation of heart Failure Treatment study (ALOFT), designed to test the safety of a directly acting renin inhibitor. Plasma aldosterone and 24-hour urinary aldosterone excretion, as well as fasting insulin and homeostasis model assessment of insulin resistance (HOMA-IR) were measured. Subjects with aldosterone escape and high urinary aldosterone were identified according to previously accepted definitions.
20% of subjects demonstrated aldosterone escape and 34% had high urinary aldosterone levels. At baseline, there was a positive correlation between fasting insulin and plasma (r = 0.22 p<0.01) and urinary aldosterone(r = 0.19 p<0.03). Aldosterone escape and high urinary aldosterone subjects both demonstrated higher levels of fasting insulin (p<0.008, p<0.03), HOMA-IR (p<0.06, p<0.03) and insulin-glucose ratios (p<0.006, p<0.06) when compared to low aldosterone counterparts. All associations remained significant when adjusted for potential confounders.
This study demonstrates a novel direct relation between aldosterone status and insulin resistance in heart failure. This observation merits further study and may identify an additional mechanism that contributes to the adverse clinical outcome associated with aldosterone escape.
Based upon epidemiological studies, male gender and younger age are risk factors for developing fatal myocarditis. The impact of age and gender on myocardial injury pattern in acute myocarditis, however, is not well understood. In patients with clinically acute myocarditis, this study sought to characterise the relation between patient age and gender and the extent of myocardial involvement using cardiovascular magnetic resonance (CMR) imaging. CMR markers for oedema, inflammation and fibrosis defined myocardial involvement.
65 patients (42 years old (SD 15), 41 male) with clinically acute myocarditis were assessed. Using standard methods, T2-weighted and contrast-enhanced T1-weighted (early and late enhancement) CMR images were acquired. T2 images were visually and quantitatively assessed for oedema. Early enhancement images were quantified for inflammation, as was regional fibrosis in late enhancement images. Data were analysed for groups of age (>40, <40 years) and gender.
62% of all patients had evidence of regional oedema, which was more prevalent in patients below 40 years of age (80.7% vs 51.3%, p<0.05), as was myocardial fibrosis (76.9% vs 48.7%, p<0.05). However, early enhancement was more frequently found in patients above 40 years (84.2% vs 61.5%, p<0.05). Men were twice as likely as women to demonstrate myocardial fibrosis (73.2 vs 37.5%, p<0.01).
In patients with clinically acute myocarditis, myocardial fibrosis was more frequent in men and in patients younger than 40 years. Injury sustained in younger patients appears to be more regional and more severe, as indicated by a higher incidence of irreversible injury.
Aortic wall pathology and concomitant aortic dilatation have been described in tetralogy of Fallot (TOF) patients, which may negatively affect aortic valve and left ventricular systolic function.
To assess aortic dimensions, aortic elasticity, aortic valve competence and biventricular function in repaired TOF patients after pulmonary valve replacement (PVR) using magnetic resonance imaging (MRI).
MRI was performed in 16 patients with TOF after PVR (10 male; mean age 31 years (SD 15)) and 16 age and gender-matched healthy subjects.
TOF patients showed aortic root dilatation (mean difference 7.8–8.8 mm, p<0.01 at all four predefined levels) and reduced aortic elasticity (pulse wave velocity in aortic arch 5.5 m/s (1.2) vs 4.6 m/s (0.9), p = 0.04; aortic root distensibility 1.4/10–3 mm Hg (1.7) vs 5.7/10–3 mm Hg (3.6), p<0.01). Minor degrees of aortic regurgitation (AR) (AR fraction 6% (8) vs 1% (1), p<0.01) and reduced left ventricular ejection fraction (LVEF) were present (51% (8) vs 58% (6), p = 0.01), whereas right ventricular ejection fraction (RVEF) was within normal limits (47% (8) vs 52% (7), p = 0.06). The degree of AR fraction was associated with dilatation of the aortic root (r = 0.39–0.49, p<0.05) and reduced aortic root distensibility (r = 0.44, p = 0.02), whereas reduced LVEF was correlated with degree of AR and RVEF (r = 0.41, p = 0.02 and r = 0.49, p<0.01, respectively).
Aortic root dilatation and reduced aortic elasticity are frequently present in patients with TOF, in addition to minor degrees of AR and reduced left ventricular systolic function. Aortic wall pathology in repaired TOF patients may therefore represent a separate mechanism leading to left ventricular dysfunction, as part of a multifactorial process of left ventricular dysfunction.
Myocardial revascularisation improves outcomes in patients with coronary artery disease. However, these procedures may themselves cause irreversible myocardial injury. The prognostic value of procedural myocardial injury is uncertain.
We quantified procedural myocardial necrosis using delayed enhancement cardiovascular magnetic resonance imaging (DE-CMR) in 152 consecutive patients before and shortly after percutaneous coronary intervention (PCI) or coronary artery bypass graft (CABG). The primary endpoint was defined as death, non-fatal myocardial infarction, sustained ventricular arrhythmia, unstable angina or heart failure requiring hospitalisation. During a median follow-up of 2.9 years, 27 patients (18%) reached the primary endpoint. 49 patients (32%) had evidence of new procedure-related myocardial hyperenhancement with a median mass of 5.0 g (interquartile range 2.7–9.8). After adjustment for age and sex, these patients had a 3.1-fold (95% confidence interval 1.4 to 6.8; p = 0.004) higher risk of adverse outcome than patients without new hyperenhancement. Cardiac troponin levels and quantitative measures of left ventricular function after procedure did not show any significant independent association with the primary endpoint and they did not alter the independent association of new hyperenhancement.
Myocardial injury during PCI or CABG, identified by DE-CMR, adversely affects clinical outcome. This suggests the benefits from revascularisation could partially be offset by new myocardial injury caused by the intervention itself.
To describe clinical features, morphology, management and outcome of pulmonary vein stenosis (PVS) in childhood.
Retrospective international collaborative study involving 19 paediatric cardiology centres in the UK, Ireland and Sweden.
Cases of PVS presenting between 1 January 1995 and 31 December 2004 were identified. Cases where pulmonary veins connected to a morphological left atrium were included. Functionally univentricular hearts and total anomalous pulmonary venous connection were excluded. All available data and imaging were reviewed.
58 cases were identified. In 22 cases (38%) there was premature delivery. 46 (79%) had associated cardiac lesions; 16 (28%) had undergone previous cardiac surgery before PVS diagnosis. 16 children (28%) had a syndrome or significant extracardiac abnormality. 36 presented with unilateral disease of which 86% was on the left. Where there was adequate sequential imaging, disease progression was shown with discrete stenosis leading to diffusely small pulmonary veins. Collateral vessels often developed. 13 patients had no intervention. Initial intervention was by catheter in 17 and surgery in 28. Overall 3-year survival was 49% (95% CI 35% to 63%) with patients undergoing initial surgical intervention having greater freedom from death or re-intervention (hazard ratio 0.44, 95% CI 0.2 to 0.99, p = 0.023).
PVS is a complex disease of uncertain cause and frequently associated with prematurity. Early intervention may be indicated to deter irreversible secondary changes.