bluuebunny/crossref_metadata_2025_split huggingface dataset:
P3391Cholesterol crystals in culprit coronary artery with acute myocardial infarction and their relation to myocardial salvage
Authors: Nunohiro T , Kuwasaki S , Fukushima T , Furudono S , Suenaga H , Takeshita S , Nakashima H 
Published: October 2019

Abstract

The involvement of cholesterol crystals (CCs) in plaque progression and destabilization of atherosclerotic plaques has been recently recognized. However, little is known about CCs and myocardial salvage in the Acute myocardial infarction (AMI) patients. This study aimed to evaluate the association between the existence of CCs at the site of culprit coronary artery and myocardial salvage index (MSI).To investigate, we applied the diagnostic resources of Optical Coherence Tomography (OCT).

Methods
This study included 53 AMI patients (90% with STEMI) who underwent primary PCI within 24h of onset. 53 STEMI patients underwent magnetic resonance imaging (CMR) of 5th days and 3 months after PCI. Infarct size was measured on delayed-enhancement imaging, and area at risk was quantified on T2-weighted imaging. MSI was calculated as [area at risk − infarct size] × 100/area at risk. 3 months CMR with contrast-enhanced imaging of late gadolinium enhancement-LGE. Patients were divided 2 groups according to the existence of CCs at the site of culprit coronary artery.

Results
CCs occurs in 26 of 53 (49%). Acute 5th days risk area (13.5±4.1 vs 12.6±4.9, P=0.48) and 3months infarct size (5.3±3.5 vs 7.0±3.2, P=0.066) were not significant between CCs and no CCs group. But salvage index were significantly lower in patients with CCs group (47.7±17.5% vs 60.1±20.2%, P=0.021)

Conclusion
Salvage index in patients that CCs were found by the OCT analysis, remain low after AMI. This study demonstrates the potential correlation between the myocardial salvage and vulnerable morphological features of culprit lesion to the presence of CCs with AMI patients.
P3395Arrival time at hyperemia of below the ankle as a determinant factor for limb salvage: evaluation by 2 dimension perfusion angiography
Authors: Ikeoka K , Watanabe T , Shinoda Y , Inui H , Fukuoka H , Ueno K , Hoshida S 
Published: October 2019

Abstract

Background
In patients with critical limb ischemia, it is desirable to obtain enough skin perfusion pressure (SPP) levels through revascularization. 2D-perfusion angiography is an emerging technology for the quantification of tissue perfusion consisted of 6 parameters calculated by time-density curve of digital subtraction angiography (DSA).

Purpose
We evaluated the feasibility of 2D-perfusion angiography for below the knee (BTK) endovascular therapy (EVT). We aimed to clarify which angiographical parameters of lower limb are related to SPP after EVT.

Methods
Consecutive 33 limbs (mean age 74.5 years, men 55%), which successfully underwent EVT for isolated BTK lesions, were enrolled in this study. We excluded Rutherford 6 limbs with severe gangrene or tissue loss, consequently 26 limbs were Rutherford 4 or 5 critical limb ischemia. We treated total 47 lesions, including 26 chronic total occlusive lesions. 5Fr guiding sheath was advanced to popliteal artery. DSA images were obtained by mechanical contrast infusion. We quantified indexed blood flow on below the ankle area by using 2D-perfusion angiography, and examined 6 parameters [arrival time (AT), time to peak (TTP), wash-in rate, width, area under the curve and mean transit time (MTT)] from acquired DSA. Hyperemia was induced by 20mg papaverine intra-arterial infusion through the guiding sheath.

Results
The parameters except wash-in rate were significantly shortened after hyperemia induced by intra-arterial papaverine infusion below the ankle region. Dorsal and plantar SPP were significantly correlated with hyperemic AT, hyperemic wash-in rate and AT ratio (hyperemic/rest) of lower ankle regions after EVT. However, only AT ratio was independently associated with dorsal SPP in multivariate analysis (P=0.032). A receiver operating characteristic curve showed hyperemic AT <4.5 seconds and AT ratio <0.49 predicted to obtain SPP levels >50 mmHg after EVT with the area under the curve of 0.71 (95% confidence interval, 0.52–0.90) and 0.73 (95% confidence interval, 0.55–0.90), respectively.
Representative Case of 2D-perfusion

Conclusion
Hyperemic AT <4.5 seconds and AT ratio <0.49 of lower ankle regions may be essential to obtain the sufficient levels of SPP for limb salvage after BTK intervention. 2D perfusion angiography technique at hyperemic condition is feasible and has the potential to monitor lower limb tissue perfusion through EVT and to optimize the interventional treatment.
P3406Validation of atherothrombotic risk score for secondary prevention in patients with acute myocardial infarction: the J-MINUET study
Authors: Hashimoto T , Ako J , Nakao K , Ozaki Y , Kimura K , Noguchi T , Suwa S , Fujimoto K , Nakama Y , Morita T , Shimizu W , Saito Y , Hirohata A , Ogawa H , Ishihara M 
Published: October 2019

Abstract

Background
Thrombolysis in Myocardial Infarction (TIMI) Risk Score for Secondary Prevention and CREDO-Kyoto Thrombotic Risk Score are contemporary secondary prevention risk scoring systems. However, these scoring systems have not been validated in other populations.

Purpose
The aim of this study was to validate of the TIMI Risk Score for Secondary Prevention and CREDO-Kyoto Thrombotic Risk Score in patients in the early phase of acute myocardial infarction (AMI).

Methods
The Japanese registry of acute Myocardial INfarction diagnosed by Universal dEfiniTion (J-MINUET) is a prospective multicenter registry conducted in 28 Japanese medical institutions. We enrolled 3,283 consecutive patients with AMI who were admitted to participating institutions within 48 hours of symptom onset between July 2012 and May 2014. Among them, 3,070 patients were included in this study after excluding 213 patients who died in the hospital. Clinical follow-up data were obtained up to 3 years. The primary endpoint was a composite of all-cause death, non-fatal MI and non-fatal stroke. The patients were stratified by the TIMI Risk Score for Secondary Prevention and CREDO-Kyoto Thrombotic Risk Score.

Results
At the 3-year follow-up, the primary endpoint had occurred in 337 patients (11.0%). All-cause death, non-fatal MI and non-fatal stroke had occurred in 177 (5.8%), 80 (2.6%) and 80 (2.6%) patients, respectively. TIMI Risk Score for Secondary Prevention and CREDO-Kyoto Thrombotic Risk Score showed a graded association with the composite of all-cause death, non-fatal MI and non-fatal stroke at 3 years in the J-MINUET population (Figure).
Validation of atherothrombotic risk

Conclusions
TIMI Risk Score for Secondary Prevention and CREDO-Kyoto Thrombotic Risk Score were shown to be applicable to the patients in the early phase of AMI.
P3411Prevalence and risk factors of multifocal cardiovascular calcification in patients at high cardiovascular risk
Authors: Van 'T Klooster C C , Nathoe H M , Leiner T , Hjortnaes J , Bots M L , Isgum I , Lessmann N , Van Der Graaf Y , Visseren F L J 
Published: October 2019

Abstract

Background
Cardiovascular calcification is associated with a higher risk for cardiovascular disease (CVD). The pathophysiology of calcium deposition is different for arteries and heart valves, and is not yet completely understood.

Purpose
The aim of the present study is to determine the prevalence of coronary artery calcification (CAC), thoracic aorta calcification (TAC) (including ascending aorta, aortic arch, and descending aorta), mitral annulus calcification (MAC), and aortic valve calcification (AVC), and to compare the associations with predetermined cardiovascular risk factors, in patients at high cardiovascular risk.

Methods
Computed tomography imaging was performed in 645 patients with stable CVD or marked risk factors, visualizing heart and thoracic aorta. Prevalence of site-specific and multifocal calcification was determined. To quantify the association of risk factors with cardiovascular calcification per location, ordinal regression analyses were performed. 99% confidence intervals were estimated to account for multiple testing.

Results
Prevalence of CAC, TAC, MAC, and AVC was 82%, 65%, 13%, and 48% respectively. Patients with MAC were most likely to have calcification in other locations simultaneously (Table 1). Age was associated with calcification in all locations (lowest OR 2.18; 99%CI 1.58–3.05 for ascending aorta calcification), and number of packyears with vascular calcification (lowest OR 1.26; 99%CI 1.03–1.54 for CAC). Diabetes mellitus and systolic blood pressure were associated with TAC, whereas waist circumference and male sex were determinants of CAC (Figure 1).
Prevalence of calcification per site Coronary artery calcification (CAC) Mitral annulus calcification (MAC) Aortic valve calcification (AVC) Thoracic aorta calcification (TAC) N=524 N=83 N=306 par N=415 No calcification in other locations (%) 103 (20%) 1 (1%) 7 (2%) 27 (7%) CAC (%) NA 77 (93%) 286 (94%) 373 (90%) MAC (%) 77 (15%) NA 67 (22%) 76 (18%) AVC (%) 286 (55%) 67 (81%) NA 256 (62%) TAC (%) 373 (72%) 76 (92%) 256 (84%) NA Prevalence of calcification is shown for patients with presence of CAC, MAC, AVC, or TAC. For example; 103 (20%) of the patients with CAC have no calcification in other studied locations, and 77 (15%) of the patients with CAC have MAC as well.
Determinants of calcification per site

Conclusion
Arterial and heart valve calcifications are generally multifocal in a population at high vascular risk. Age was the only consistent risk factor. Differences in association with cardiovascular risk factors imply limited influence of atherosclerotic pathways in heart valve calcification compared to vascular calcification, and suggest more pronounced tunica media involvement in TAC than in CAC.
P3422Contrasting the risk for atherosclerotic cardiovascular disease events among individuals with lower extremity peripheral artery disease, coronary heart disease and cerebrovascular disease
Authors: Hubbard D , Colantonio L D , Rosenson R S , Brown T M , Jackson E A , Dai Y , Mues K E , Woodward M , Muntner P M , Farkouh M E 
Published: October 2019

Abstract

Background
Having more vascular conditions, including coronary heart disease (CHD), cerebrovascular disease and lower extremity artery disease (LEAD), may increase the risk for atherosclerosis cardiovascular disease (ASCVD) events. Specific vascular conditions may increase the ASCVD event rate more than others.

Purpose
To compare the risk for future ASCVD events associated with the number and type of vascular conditions among adults with a history of CHD, cerebrovascular disease and/or LEAD.

Methods
We analyzed data from US adults ≥19 years of age with commercial or Medicare health insurance who had a history of CHD, cerebrovascular disease and/or LEAD as of December 31, 2014 (N=901,391). Individuals were followed through December 31, 2016 (median follow-up: 2 years) for ASCVD events, including myocardial infarction, coronary revascularization, stroke, carotid revascularization and lower extremity amputation or revascularization.

Results
Among individuals included in the current analysis (mean age 63 years, 45% female), 70%, 23% and 7% had 1, 2 and 3 vascular conditions, respectively. After adjustment for sociodemographic and cardiovascular risk factors, the hazard ratio for ASCVD among individuals with 2 and 3 versus 1 vascular conditions was 1.88 (1.85, 1.92) and 2.93 (2.86, 3.00), respectively. Among individuals with 1 vascular condition, the rate of ASCVD events per 1,000 person-years was 46.5 (95% CI 44.1, 49.0), 29.6 (95% CI 29.0, 30.1) and 19.9 (95% CI 19.2, 20.8) for those with LEAD, CHD and cerebrovascular disease, respectively. The multivariable-adjusted hazard ratio (95% CI) for ASCVD events comparing individuals with LEAD only and CHD only versus those with cerebrovascular disease only was 1.84 (1.77, 1.92) and 1.12 (1.08, 1.16), respectively. Among individuals with 2 vascular conditions, the ASCVD event rate per 1,000 person-years was higher in those with LEAD and CHD (122.0, 95% CI 112.5, 132.2) and with LEAD and cerebrovascular disease (92.4, 95% CI 79.9, 106.4), versus those with CHD and cerebrovascular disease (59.1, 95% CI 54.8, 63.6). The multivariable-adjusted hazard ratio (95% CI) comparing individuals with LEAD and CHD and those with LEAD and cerebrovascular disease versus those with CHD and cerebrovascular disease was 1.48 (1.44, 1.53) and 1.49 (1.41, 1.58), respectively.

Conclusion
Among adults with vascular disease, having LEAD confers a higher risk for future ASCVD events than CHD or cerebrovascular disease and this group may benefit from more intensive risk reduction treatment.

Acknowledgement/Funding
Amgen Inc.
P3423The contribution of genetics to premature CAD through different degrees of lifestyle factors: a matter of relative significance?
Authors: Sousa J , Mendonca M , Pereira A , Mendonca F , Neto M , Monteiro J , Sousa A C , Rodrigues M , Henriques E , Guerra G , Borges S , Ornelas I , Drumond A , Palma Dos Reis R 
Published: October 2019

Abstract

Introduction
Coronary artery disease (CAD) is a multifactorial process with substantial genetic contribution. However, genetic predisposition among patients with a different number of lifestyle factors and premature CAD, remains a complex and thoroughly unexplored topic.

Objective
To evaluate, in a young population, the importance of conventional risk factors as well as of a genetic risk score in the appearance of CAD.

Methods
A case-control study was conducted with 1075 patients from the GENEMACOR study population, under 50 years-old (555 cases, 86.8% male, mean age 44.1±4.9 years and 520 controls, 86.2% male, mean age 44.3±4.8 years). Univariate analysis addressed the association of different modifiable risk factors with premature CAD. Genetic risk score (GRS) was computed comprising 33 genetic risk variants in a multiplicative method. GRS was evaluated according to the number of traditional risk factors and risk for premature CAD was estimated and its independent predictive value estimated by logistic regression.

Results
72.6% of patients had ≥3 risk factors vs 31.2% of controls (p<0.0001). In comparison with having no risk factors (rf), patients with 1 rf had an OR of 2.79 (1.19–6.53; p=0.015), patients with 2 risk factors had a OR of 6.87 (3.03–15–57, p<0.0001) and patients with 3 modifiable risk factors had a OR of 24.17 (10.87–53.73, p<0.0001) – graph 1. In this young population, mean GRS level was consistently higher among patients with coronary artery disease comparing with a healthy population (0.6±0.6 vs 0.4±0.4, p<0.0001, respectively) – graph 2. GRS in multivariate analysis, proved to be an independent predictor for premature CAD (OR 1.71, CI95% 1.25–2.34, p=0.001).

Conclusion
In our population, GRS was an independent predictor for premature CAD. In young patients with ≥3 risk factors, genetics play a less decisive role in the development of CAD. Even in young patients, modifiable risk factors should be addressed aggressively as they may represent a higher burden than genetic predisposition itself.
P3429A novel prediction model for mortality after cardiac surgery using institutional case volume
Authors: Lee S , Park J B , Cho Y J , Ryu H G , Jang E J 
Published: October 2019

Abstract

Purpose
A number of risk prediction models have been developed to identify short term mortality after cardiovascular surgery. Most models include patient characteristics, laboratory data, and type of surgery, but no consideration for the amount of surgical experience. With numerous reports on the impact of case volume on patient outcome after high risk procedures, we attempted to develop a risk prediction models for in-hospital and 1-year mortality that takes institutional case volume into account.

Methods
We identified adult patients who underwent cardiac surgery from January 2008 to December 2017 from the National Health Insurance Service (NHIS) database by searching for patients with procedure codes of coronary artery bypass grafting, valve surgery, and surgery on thoracic aorta during the hospitalization. Study subjects were randomly assigned to either the derivation cohort or the validation cohort. In-hospital mortality and 1-year mortality data were collected using the NHIS database. Risk prediction models were developed from the derivation cohort using Cox proportional hazards regression. The prediction performances of models were evaluated in the validation cohort.

Results
The models developed in this study demonstrated fair discrimination for derivation cohort (N=22,004, c-statistics, 0.75 for in-hospital mortality; 0.73 for 1-year mortality) and acceptable calibration in the validation cohort. (N=22,003, Hosmer-Lemeshow χ2-test, P=0.08 and 0.16, respectively). Case volume was the key factor of mortality prediction models after cardiac surgery. (50≤ x <100 case per year. 100≤ x <200 case per year, ≥200 case per year are correlated with OR 3.29, 2.49, 1.85 in in-hospital mortality, 2.76, 1.99, 1.69 in 1-year mortality respectively, P value <0.001.)
Annual case volume as risk factor Variables In-hospital mortality 1-year mortality OR (95% CI) p-value OR (95% CI) p-value Annual case-volume (reference: ≥200) – – 100–200 1.69 (1.48, 1.93) <0.001 1.85 (1.58, 2.18) <0.001 50–100 1.99 (1.75, 2.25) <0.001 2.49 (2.15, 2.89) <0.001 <50 2.76 (2.44, 3.11) <0.001 3.29 (2.85, 3.79) <0.001 OR: Odds ratio; CI: confidence interval; Ref: Reference.
Discrimination and calibration

Conclusion
We developed and validated new risk prediction models for in-hospital and 1-year mortality after cardiac surgery using the NHIS database. These models may provide useful guides to predict mortality risks of patients with basic information and without laboratory findings.
P3438Malaria infection and risk of incident heart failure: a nationwide cohort study
Authors: Brainin P , Mohr G H , Modin D , Claggett B , Silvestre O M , Shah A , Hviid L , Pedersen C T , Kober L , Solomon S , Schou M , Gislason G H , Biering-Sorensen T 
Published: October 2019

Abstract

Background
Malaria is a parasitic mosquito-borne infection which affects more than 219 million people worldwide each year. Recent studies have hypothesized that malaria may contribute to functional and structural changes in the myocardium, which can lead to cardiovascular disease. We therefore investigated the risk of heart failure (HF) and other cardiovascular events in individuals with a prior history of malaria infection.

Methods
Danish nationwide registries were used to identify patients with a history of malaria infection between January 1994 and January 2017. Patients with ischemic heart disease or HF at baseline were excluded. The population was sex and age matched with the general population in a ratio of 1:10. Information on cardiovascular risk factors and medication were assessed at time of the malaria diagnosis. Cox proportional hazards models, and a propensity score-matched model, were used to assess the risk of HF, myocardial infarction (MI) and cardiovascular death (CVD).

Results
A total of 3,570 malaria cases were identified (40% had plasmodium falciparum). The median age was 32 years and 57% were male. During a median follow-up time of 11 years [interquartile range 5, 17], 52 cases experienced incident HF (1.5%), 30 MI (0.9%) and 58 suffered from CVD (1.6%). In unadjusted survival analyses, malaria cases had a significantly increased risk of HF (HR 1.34 95% CI 1.01–1.79, P=0.046) but not MI (HR 0.72 95% CI 0.51–1.03, P=0.073) or CVD (HR 1.14 95% CI 0.87–1.49, P=0.34). In multivariable models adjusted for hypertension, diabetes, chronic kidney disease, vascular disease and concomitant pharmacotherapy (lipid lowering/antianginal/diuretics/betablocker), the association with HF remained significant (HR 1.40 95% CI 1.05–1.87, P=0.023). A propensity score-matched model based on 7,152 individuals (1:1 of cases and controls) also yielded a significant association with HF (HR 1.59 95% CI 1.03–2.46, P=0.036).
Forest plot: Malaria and CV events

Conclusion
Our data indicate that individuals with a prior history of a malaria infection may have an increased risk of incident HF but not MI or CVD. This suggests that malaria, on a hypothesis-generating basis, may affect long-term cardiac function.
P3439Causes of death in patients with chronic myocardial injury
Authors: Roos A , Kadesjo E , Sartipy U , Holzmann M J 
Published: October 2019

Abstract

Background/Introduction
Persistently elevated high-sensitivity cardiac troponin T (hs-cTnT) levels above the 99th percentile value indicate ongoing chronic myocardial injury which is associated with a high risk of death, heart failure, and myocardial infarction. No prior studies have thoroughly investigated the causes of death in patients with chronic myocardial injury.

Purpose
To investigate causes of death in patients with chronic myocardial injury.

Methods
In a cohort of 19,460 consecutive patients with chest pain and stable hs-cTnT levels measured concurrently from 2011 to 2014 at the Karolinska university hospital, of whom 1528 (7.9%) had myocardial injury, we included all patients who died during a mean follow-up of 4.0±1.3 years. Incidence rates for cause-specific deaths were calculated within following categories of hs-cTnT levels: <5, 5–9, 10–14, 15–29, 30–49, and ≥50 ng/l. Logistic regression was used to estimate adjusted odds ratios (OR) with 95% confidence intervals (CI) for the association between hs-cTnT levels and the relation between cardiovascular (CV) and non-cardiovascular (non-cardiovascular) causes of death, for patients with hs-cTnT levels of 5–14, and >14 ng/l, respectively using patients with hs-cTnT levels <5 ng/l as referent.

Results
In total, 1577 patients (8.1%) were included, of whom 684 (43%) had chronic myocardial injury (i.e. hs-cTnT >14 ng/l). Higher hs-cTnT levels were associated with higher age at baseline and at death, male sex, kidney dysfunction and comorbidities. The yearly cardiovascular and non-cardiovascular death rates increased with increasing hs-cTnT levels from 0.07% and 0.4% (<5 ng/l), to 17% and 15% (≥50 ng/l), respectively. Corresponding rates for cancer death increased from 0.6% to 4.0%. The proportion of cardiovascular versus non-cardiovascular deaths increased with hs-cTnT levels (figure). Patients with hs-cTnT levels 5–14 ng/l were 87% more likely to die from cardiovascular causes compared with patients with hs-cTnT <5 ng/l (adjusted OR: 1.87, 95% CI: 1.24–2.80), while the risk was doubled in those with chronic myocardial injury (adjusted OR: 2.02, 95% CI: 1.29–3.15). The proportion of patients suffering from cardiovascular death increased with age in both women and men.
Causes of Death

Conclusions
We found a gradual increase in the risk of cardiovascular death with increasing hs-cTnT levels, already below the 99th percentile value. Patients with chronic myocardial injury were twice as likely to die from cardiovascular causes compared with patients with undetectable troponin levels, with almost half of the patients dying cardiovascular death. Chronic myocardial injury is associated with a high risk of cardiovascular death.

Acknowledgement/Funding
None