Epicardial adipose tissue volume, plaque vulnerability and myocardial ischemia in non-obstructive coronary artery disease.

Background: Epicardial adipose tissue (EAT) accumulation has been associated with inflammation, atherosclerosis and microvascular dysfunction. Whether increased EAT volume is associated with coronary plaque vulnerability and demand myocardial ischemia in patients with non-obstructive coronary artery disease (CAD) is less explored. Methods: In 125 patients (median age 63[58, 69] years and 58% women) with chest pain and non-obstructive CAD, EAT volume was quantified on non-contrast cardiac CT images. EAT volume in the highest tertile (>125 ml) was defined as high EAT volume. Total coronary plaque volume and plaque vulnerability were quantified by coronary CT angiography (CCTA). Demand myocardial ischemia was detected by contrast dobutamine stress echocardiography. Results: High EAT volume was more common in men and associated with higher BMI, hypertension, increased left ventricular mass index (LVMi), C-reactive protein (CRP) and positive remodelling (all p < 0.05). There was no difference in age, coronary calcium score, total and non-calcified plaque volume or presence of demand myocardial ischemia between groups (all p ≥ 0.34). In a multivariable model, obesity (p = 0.006), hypertension (p = 0.007) and LVMi (p = 0.016) were independently associated with high EAT volume. Including plaque vulnerability in an alternative model, positive remodelling (p = 0.038) was independently associated with high EAT volume. Conclusion: In non-obstructive CAD, high EAT volume was associated with cardiometabolic risk factors, inflammation and plaque vulnerability, while there was no association with demand myocardial ischemia or coronary plaque volume. Following our results, the role of EAT volume as a biomarker in non-obstructive CAD remains unclear.

Relationship between hypertension and non-obstructive coronary artery disease in chronic coronary syndrome (the NORIC registry).

BACKGROUND: The burden of non-obstructive coronary artery disease (CAD) in the society is high, and there is currently limited evidence-based recommendation for risk stratification and treatment. Previous studies have demonstrated an association between increasing extent of non-obstructive CAD and cardiovascular events. Whether hypertension, a modifiable cardiovascular risk factor, is associated with extensive non-obstructive CAD in patients with symptomatic chronic coronary syndrome (CCS) remains unclear. METHODS: We included 1138 patients (mean age 62±11 years, 48% women) with symptomatic CCS and non-obstructive CAD (1-49% lumen diameter reduction) by coronary computed tomography angiography (CCTA) from the Norwegian Registry for Invasive Cardiology (NORIC). The extent of non-obstructive CAD was assessed as coronary artery segment involvement score (SIS), and extensive non-obstructive CAD was adjudicated when SIS >4. Hypertension was defined as known hypertension or use of antihypertensive medication. RESULTS: Hypertension was found in 45% of patients. Hypertensive patients were older, with a higher SIS, calcium score, and prevalence of comorbidities and statin therapy compared to the normotensive (all p<0.05). There was no difference in the prevalence of hypertension between sexes. Univariable analysis revealed a significant association between hypertension and non-obstructive CAD. In multivariable analysis, hypertension remained associated with extensive non-obstructive CAD, independent of sex, age, smoking, diabetes, statin treatment, obesity and calcium score (OR 1.85, 95% CI [1.22-2.80], p = 0.004). CONCLUSION: In symptomatic CCS, hypertension was associated with extensive non-obstructive CAD by CCTA. Whether hypertension may be a new treatment target in symptomatic non-obstructive CAD needs to be explored in future studies. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov: Identifier NCT04009421.

Total coronary atherosclerotic plaque burden is associated with myocardial ischemia in non-obstructive coronary artery disease.

AIM: Whether the total coronary atherosclerotic plaque burden is independently associated with myocardial ischemia in non-obstructive coronary artery disease (CAD) is not well established. We aimed to test the association of total plaque burden quantified by coronary computed tomography angiography (CCTA) with myocardial ischemia in patients with chronic coronary syndrome and non-obstructive CAD. METHODS: We included 125 patients (age 62 ± 9 years, 58% women) with chronic coronary syndrome and non-obstructive CAD (stenosis < 50%) by CCTA, who were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. Total plaque burden was quantified by CCTA as the total plaque volume in the main coronary arteries, and positive remodelling was defined as remodelling index > 1.10. RESULTS: Patients with myocardial ischemia (n = 66) had higher total plaque burden (847 ± 245 mm3 vs. 758 ± 251 mm3, p = 0.049) and higher left ventricular (LV) mass index (42.1 ± 9.9 g/m2.7 vs. 37.3 ± 8.0 g/m2.7, p = 0.004), while age, sex, prevalence of hypertension, diabetes, calcium score and positive remodelling did not differ between the groups (all p > 0.05). In multivariable regression analysis, total plaque burden remained associated with presence of myocardial ischemia (OR 1.02, 95% CI 1.00-1.04, p = 0.045) independent of age, sex, hypertension, diabetes, LV mass index, coronary calcium score and positive remodelling. CONCLUSION: Total coronary artery plaque burden by CCTA was independently associated with myocardial ischemia in patients with non-obstructive CAD. Whether plaque quantification is useful for clinical management of patients with non-obstructive CAD should be tested in prospective studies.ClinicalTrials.gov: Identifier NCT01853527.

Impact of aortic stiffness on myocardial ischaemia in non-obstructive coronary artery disease.

Objective: High aortic stiffness may reduce myocardial perfusion pressure and contribute to development of myocardial ischaemia. Whether high aortic stiffness is associated with myocardial ischaemia in patients with stable angina and non-obstructive coronary artery disease (CAD) is less explored. Methods: Aortic stiffness was assessed as carotid-femoral pulse wave velocity (PWV) by applanation tonometry in 125 patients (62±8 years, 58% women) with stable angina and non-obstructive CAD participating in the Myocardial Ischemia in Non-obstructive CAD project. PWV in the highest tertile (>8.7 m/s) was taken as higher aortic stiffness. Stress-induced myocardial ischaemia was detected as delayed myocardial contrast replenishment during stress echocardiography, and the number of left ventricular (LV) segments with delayed contrast replenishment as the extent of ischaemia. Results: Patients with higher aortic stiffness were older with higher LV mass index and lower prevalence of obesity (all p<0.05), while angina symptoms, sex, prevalence of hypertension, diabetes, smoking or LV ejection fraction did not differ between groups. Stress-induced myocardial ischaemia was more common (73% vs 42%, p=0.001) and the extent of ischaemia was larger (4±3 vs 2±3 LV segments, p=0.005) in patients with higher aortic stiffness. In multivariable logistic regression analysis, higher aortic stiffness was associated with stress-induced myocardial ischaemia independent of other known covariables (OR 4.74 (95% CI 1.51 to 14.93), p=0.008). Conclusions: In patients with stable angina and non-obstructive CAD, higher aortic stiffness was associated with stress-induced myocardial ischaemia. Consequently, assessment of aortic stiffness may add to the diagnostic evaluation in patients with non-obstructive CAD. Trial registration number: NCT01853527.

Left ventricular hypertrophy contributes to Myocardial Ischemia in Non-obstructive Coronary Artery Disease (the MicroCAD study).

BACKGROUND: The underlying mechanisms causing myocardial ischemia in non-obstructive coronary artery disease (CAD) are still unclear. We explored whether left ventricular hypertrophy (LVH) was associated with myocardial ischemia in patients with stable angina and non-obstructive CAD. METHODS: 132 patients (mean age 63 ±â€¯8 years, 56% women) with stable angina and non-obstructive CAD diagnosed as <50% stenosis by coronary computed tomography angiography (CCTA) underwent myocardial contrast stress echocardiography. Left ventricular (LV) hypertrophy (LVH) was identified by LV mass index >46.7 g/m2.7 in women and >49.2 g/m2.7 in men. Patients were grouped according to presence or absence of myocardial ischemia by myocardial contrast stress echocardiography. The number of LV segments with ischemia at peak stress was taken as a measure of the extent of myocardial ischemia. RESULTS: Myocardial ischemia was found in 52% of patients, with on average 5 ±â€¯3 ischemic LV segments per patient. The group with myocardial ischemia had higher prevalence of LVH (23 vs. 10%, p = 0.035), while age, sex and prevalence of hypertension did not differ between groups (all p > 0.05). In multivariable regression analyses, LVH was associated with presence of myocardial ischemia (odds ratio 3.27, 95% confidence interval [1.11-9.60], p = 0.031), and larger extent of myocardial ischemia (ß = 0.22, p = 0.012), independent of confounders including age, hypertension, obesity, hypercholesterolemia, calcium score and segment involvement score by CCTA. CONCLUSIONS: LVH was independently associated with both presence and extent of myocardial ischemia in patients with stable angina and non-obstructive CAD by CCTA. These results suggest LVH as an independent contributor to myocardial ischemia in non-obstructive CAD. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov, identifier NCT018535271.

Are participants in the Medical Student Research Programme continuing to engage in research? / Fortsetter forskerlinjestudenter å forske?

BAKGRUNN: I 2002 ble Forskerlinjen opprettet for tidlig å rekruttere medisinstudenter til forskning. Vi ønsket å kartlegge hvor mange tidligere forskerlinjestudenter fra Universitetet i Bergen som fortsatte å forske og identifisere faktorer som var assosiert med videre forskning. MATERIALE OG METODE: Alle studenter innrullert i forskerlinjeprogrammet ved Universitetet i Bergen siden oppstart i 2002 som var uteksaminert fra medisinstudiet innen juni 2017 ble kontaktet per e-post med en elektronisk spørreundersøkelse. Vi undersøkte om deltagerne holdt på med eller hadde gjennomført doktorgrad, antall publiserte artikler, tid siden siste publisering, akademisk undervisning og veiledning samt nåværende stilling på universitet eller høyskole. RESULTATER: Totalt 102 av 148 (69 %) besvarte spørreundersøkelsen. Av disse hadde 68 % gått videre med doktorgrad, 38 % var involvert i akademisk undervisning eller veiledning og 29 % var ansatt i en akademisk stilling. Samlet hadde deltagerne i median publisert fire artikler. Kvinner hadde større sannsynlighet for å gå videre med doktorgrad enn menn. Det samme hadde de som publiserte minst én artikkel før fullført medisinstudium, og de som ikke hadde mottatt regelmessig veiledning som forskerlinjestudent. Det var ingen sammenheng mellom det å fullføre Forskerlinjen og det å gå videre med doktorgrad. FORTOLKNING: Mange medisinstudenter som har gått Forskerlinjen ved Universitetet i Bergen fortsetter med forskning etter fullført studium. Dette gjelder også de som ikke fullfører linjen.

Global Coronary Artery Plaque Area is Associated with Myocardial Hypoperfusion in Women with Non-ST Elevation Myocardial Infarction.

BACKGROUND: Women with non-ST elevation myocardial infarction (NSTEMI) have similar extent of myocardial ischemia but less obstructive coronary artery disease (CAD) than their male counterparts. We tested the impact of global coronary artery plaque area and artery tortuosity on myocardial perfusion in NSTEMI patients. METHODS: Coronary artery plaque area was determined by quantitative angiography in 108 patients (32% women) with NSTEMI. Myocardial perfusion was assessed by contrast echocardiography in the 17 individual left ventricular segments. Artery tortuosity was defined as ≥3 curves >45° in a main coronary artery. RESULTS: Age, prevalence of hypertension, and diabetes did not differ between sexes (all nonsignificant). Women had lower prevalence of ≥50% coronary artery stenosis (74% vs. 91%, p<0.05), while global coronary plaque area (35±22 vs. 43±21mm(2)) and the number of segments with hypoperfusion (6.9±3.7 vs. 7.2±3.4) did not differ between sexes (both p>0.07). In multivariate analysis, larger coronary artery plaque area was associated with a 35% higher risk for having severe myocardial hypoperfusion (odds ratio 1.35 [95% confidence interval 1.01-1.80], p<0.05) in the total study population, while no association between artery tortuosity and myocardial ischemia was found. Similar results were obtained in separate analysis among women and men. CONCLUSION: In women and men with NSTEMI, the global coronary artery plaque area was an important determinant of the severity of myocardial hypoperfusion at rest independent of presence of significant coronary stenoses. These findings may expand current understanding of NSTEMI in patients with nonobstructive CAD.