Progression Of Coronary Lesions Research Articles

Coronary artery culprit lesions progression and ambient temperature exposure - personalised analysis.

Global warming is claimed to be an important cardiovascular disease risk factor. The air pollution and ambient temperatures are believed to have a significant influence on increased morbidity and premature deaths. To point out possible causative factors for coronary angiography progression in patients presenting with chronic coronary syndrome. There were 66 patients (41 [62%] men and 25 [38%] women) with a median age of 71.5 (62-76) years, who underwent repeated coronary angiographies due to chronic coronary syndrome within a median time interval of 145 (96-296) days. In 18 (27%) patients coronary artery lesion progression was observed despite optimal pharmacotherapy. The demographical, clinical, and personalised epidemiological factors including air pollution particles and ambient temperature exposure were taken into account in the analysis. In the multivariate logistic regression model with backward stepwise elimination method, tropical nights (p = 0.047) and mean daily temperatures (p = 0.043) were revealed as predictors of coronary lesion progression > 30%. The analysis of seasonal temperature changes showed significant differences related to minimal winter temperatures between both groups (p = 0.018). Coronary artery lesion progression can be related to either high values of daily temperatures or to low ambient temperature. The dichotomous characteristics of temperature exposure to atherosclerosis progression suggest a detrimental role of environmental extremities on human health.

Impact of Radial Wall Strain on Serial Changes in Vascular Physiology in Patients with Intermediate Coronary Stenosis.

Coronary biomechanical stress contributes to the plaque rupture and subsequent events. This study aimed to investigate the impact of plaque biomechanical stability on the physiological progression of intermediate lesions, as assessed by the radial wall strain (RWS) derived from coronary angiography. Patients with at least one medically treated intermediate lesion at baseline who underwent follow-up coronary angiography over 6 months were included. The maximal RWS ( ) of the interrogated lesion was calculated from the baseline angiogram. The primary endpoint was to determine the association between baseline and the functional progression of coronary lesions, defined as an increase in the lesion-specific quantitative flow ratio (L- QFR, calculated as the absolute change in QFR across the lesion) on serial angiograms. Among 175 lesions in 156 patients, 63 lesions showed an increase in L- QFR during a median follow-up period of 12.4 months. Baseline values were significantly higher in lesions with increased L- QFR than in those with stabilized or decreased L- QFR (11.8 [10.7, 13.7] vs.10.8 [9.7, 11.7]; p 0.001). Baseline presented an area under the curve of 0.658 (95% confidence interval [CI]: 0.572-0.743, p 0.001) for the prediction of increased L- QFR. After full adjustment for clinical and angiographic factors, a high ( 12) was found to be an independent predictor of functional lesion progression (odds ratio: 2.871, 95% CI: 1.343-6.138, p = 0.007). A high calculated from baseline angiograms was independently associated with the subsequent physiological progression in patients with intermediate coronary lesions.

Predictors of Inappropriately Rapid Coronary Lesion Progression in Patients Undergoing Percutaneous Coronary Interventions

BackgroundPatients undergoing percutaneous coronary intervention (PCI) may experience rapid atherosclerotic plaque progression in nontreated vessels that is unlikely to result from natural de novo atherosclerosis. We hypothesize that intra-lesion bleeding plays a central role in this process. The aim of this study is to investigate the factors that may contribute to accelerated narrowing in coronary diameter. MethodsWe reviewed 65 interventional procedures and their consequent staged PCIs and mapped the coronary tree into 16 segments (as divided by the American Heart Association), grading the percentage of stenosis in each segment and spotting the rapidly progressing lesions. Demographic, procedural, and laboratory data were recorded and analyzed. ResultsFor the lesions that progressed rapidly in the time period between angiographies, the administration of eptifibatide intra-procedurally was associated with rapid progression of coronary lesions. Moreover, an increased white blood cell count prior to the index procedure was also associated with a trend toward rapid plaque progression. ConclusionsIn this hypothesis-generating study, treatment with a IIb/IIIa inhibitor in the index PCI was associated with an accelerated short-term progression of some of the nontreated lesions, suggesting that this mode of anti-aggregation therapy could facilitate plaque hemorrhage and consequent acceleration of coronary atherosclerosis in eroded plaques.

Angiography-derived radial wall strain predicts coronary lesion progression in non-culprit intermediate stenosis.

Intermediate coronary lesions (ICLs) are highly prevalent but ported mixed prognosis. Radial strain has been associated with plaque vulnerability, yet its role in predicting lesion progression is largely unknown. The purpose of this study was to determine the predictive value of angiography-derived radial wall strain (RWS) for progression of untreated non-culprit ICLs. Post-hoc analysis was conducted in a study cohort including 603 consecutive patients with 808 ICLs identified at index procedure with angiographic follow-up of up to two years. RWS analysis was performed on selected angiographic frames with minimal foreshortening and vessel overlap. Lesion progression was defined as ≥ 20% increase in percent diameter stenosis. Lesion progression occurred in 49 ICLs (6.1%) with a median follow-up period of 16.8 months. Maximal RWS (RWSmax), frequently located at the proximal and throat plaque regions, distinguished progressive ICLs from silent ones. The largest area under the curve value of 0.75 (95% CI: 0.67-0.82, P < 0.001) was reached at the optimal RWSmax cutoff value of > 12.6%. According to this threshold, 178 ICLs were classified as having a high strain pattern. Exposure to a high strain amplitude with RWSmax > 12.6% was independently associated with an increased risk of lesion progression (adjusted HR = 6.82, 95% CI: 3.67-12.66, P < 0.001). Assessment of RWS from coronary angiography is feasible and provides independent prognostic value in patients with untreated ICLs.

Association between Carotid Intraplaque Neovascularization Detected by Contrast-Enhanced Ultrasound and the Progression of Coronary Lesions in Patients Undergoing Percutaneous Coronary Intervention

It is thought that the progression of vulnerable plaque is due in part to neovascularization, and plaque vulnerability is a useful approach for classifying cardiovascular risk. The aim of this retrospective study was to evaluate the correlation between carotid intraplaque neovascularization (IPN) detected on contrast-enhanced ultrasound and the progression of coronary lesions in patients undergoing percutaneous coronary intervention (PCI). Contrast-enhanced ultrasound and angiography were performed in 131 patients undergoing PCI. All patients had angiograms obtained ≥12months after PCI, and progression was defined using those angiograms. On the basis of angiographic images, patients were divided into progression and nonprogression groups. IPN was graded from 0 to 3 according to each plaque's microbubble appearance and extent, detected using contrast-enhanced ultrasound. The plaque with the highest IPN was used for analysis. Logistic regression and receiver operating characteristic analyses were applied to evaluate risk factors for predicting the progression of coronary lesions in patients undergoing PCI. In the progression group, the numbers of patients with IPN values of 0, 1, 2, and 3 were one (3.3%), nine (30.0%), 16 (53.3%), and four (13.3%), respectively. Significant differences were found in maximum plaque height and IPN between groups. IPN and maximum plaque height were independent risk contributors to coronary lesion progression in patients undergoing PCI. The sensitivity, specificity, positive predictive value, and negative predictive value of IPN of 1.5 and to predict the progression of coronary lesions were 67%, 91%, 68%, and 89%, respectively. The area under the curve was 0.822. Carotid plaque neovascularization was correlated with the progression of coronary lesions in patients undergoing PCI. IPN is a clinically useful tool for detecting the progression of coronary lesions and for risk stratification, especially in patients >60years old.

Angiographic and Clinical Predictors of Mild Non-Culprit Coronary Lesion Progression in Acute ST-Elevation Myocardial Infarction Managed by Primary Percutaneous Coronary Intervention: A Prospective Cohort Study

Abstract Aims To identify the angiographic and clinical predictors of mild non-culprit coronary lesion (NCCL) progression in acute ST-elevation myocardial Infarction (STEMI). Methods and Results The present prospective cohort study evaluated 200 patients with acute STEMI underwent primary percutaneous coronary intervention (PPCI) (either PPCI or pharmaco-invasive PCI) divided into2groups based on whether the clinically driven non culprit lesion PCI existed or not into: Control group-1: 157 patients(78.5%) with non-progressed non culprit lesion (no additional PCI to the non-culprit lesion) and Study group-2: 43 patients(21.5%) with clinically driven non culprit lesion PCI (underwent additional PCI to progressed non-culprit lesions). Our study end point was the clinically driven non culprit lesion PCI (additional PCI to progressed non-culprit lesions). Asymptomatic patients were followed up by exercise ECG at 12 months and myocardial perfusion stress testing at 24 months. Multivariate regression analysis showed that the strongest independent predictor for progression of mild NCCL was complex morphology of culprit lesion (p &amp;lt; 0.001). Finally, a receiver operating characteristic (ROC) curve was performed to assess a cutoff value for predictors for NCCL progression after PPCI in Patients with STEMI. Conclusions Our novel angiographic independent predictor was complex morphology of culprit lesion. And our novel clinical independent predictors were CRP cutoff more than 7.05mg/l, peak cardiac troponin I value cutoff more than 27.5 ng/ml, and age cutoff less than 57.5 years, could be used for early prediction of mild NCCL progression after PPCI for acute STEMI patients. This could be used for early diagnosis to avoid repeated PCI and proper management for better outcomes.

Angiographic and clinical predictors of Non-culprit coronary Lesion Progression after Percutaneous coronary intervention in Patients with ST-Elevation Myocardial Infarction.

Background: Most of cardiovascular (CV) events in ST-elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI) are linked to the progression of non-culprit coronary lesions (NCCLs) during the follow-up period. Yet, the clinical and angiographic risk factors of non-culprit coronary lesion (NCCL) progression are not well known. Objectives: To assess the clinical risk profile and angiographic features that can be related to the progression of non-culprit lesions (NCLs) of patients with STEMI undergoing PCI over 24 months duration.Subjects and methods: The present cohort study evaluated 200 patients with STEMI underwent PCI to the culprit lesion and have mild non culprit lesion (NCL) 1.4mmol/L) (OR:54.656, 95% CI: 4.052 to 737.256; p= 0.003), Complex culprit lesion(OR:296.112, 95% CI: 13.673 to 6412.728; p < 0.001), and presence of more than one NCL (OR:22.447, 95% CI: 2.521 to 199.849; p= 0.005). Conclusion: The underlying clinical and angiographic characteristics can predict NCLs progression. Complex morphology of culprit lesion is the strongest independent predictor for progression of NCLs.

Study on Inflammation and Rehabilitation of Patients with Coronary Heart Disease after Percutaneous Coronary Intervention

In order to prevent the inflammatory reaction caused by vascular wall injury after percutaneous coronary intervention treatment, affecting the therapeutic effect and rehabilitation, this study will select 54 patients with coronary heart disease and then randomly divided them into two groups to observe and compare inflammatory factors and their connection with postoperative thrombolysis in myocardial infarction frame count, the factors include interleukin-6, interleukin-9, interleukin-17A. It has been found that part of factors was elevated after surgery of elective percutaneous coronary intervention for stable coronary heart disease patients, suggesting that percutaneous coronary intervention may induce inflammatory reactions. High level of local inflammatory factors interleukin-6, helper T cells 17 may affect the forward arterial blood flow after interventional intervention. Thrombus aspiration can reduce the occurrence of slow or no reflow in patients with thrombotic load, increase coronary perfusion, improve postoperative cardiac function, and is expected to reduce heart attacks. In patients with coronary heart disease, the expression of inflammatory factors increases with the severity of coronary heart disease and the severity of coronary atherosclerosis. The level of inflammatory factors is correlated with the degree of coronary artery disease, which may promote the progression of coronary lesions. Rehabilitation therapy of traditional Chinese and Western medicine is necessary for patients with coronary heart disease after percutaneous coronary intervention. Active rehabilitation therapy is of great significance in improving the patient’s exercise tolerance, reducing the incidence of cardiovascular adverse events, reducing complications and improving patient’s quality of life.

Cilostazol for Chinese Patients with Aspirin Intolerance after Coronary Drug-Eluting Stent Implantation

Cilostazol-based dual antiplatelet therapy (DAPT) is widely used in patients with aspirin intolerance after coronary drug-eluting stent (DES) implantation in China. However, this empirical strategy is not recommended or even mentioned in Chinese or international guidelines due to a lack of evidence from large-scale studies. We aimed to explore the efficacy and safety of cilostazol-based DAPT in this special population. In this cohort study, patients were grouped according to the DAPT strategy that they received after coronary DES implantation. The primary efficacy endpoint was major adverse cardiovascular and cerebrovascular events (MACCEs). Angiographic follow-up and major bleeding events were also recorded. A total of 918 patients receiving cilostazol-based DAPT due to aspirin intolerance were enrolled, matched with 918 patients receiving aspirin-based DAPT. After 15-month prospective follow-up, the cilostazol group had lower risk of MACCE (5.1% vs. 7.6%, propensity score adjusted hazard ratio = 0.671 [95% confidence interval 0.462-0.974], p = 0.036) compared with the aspirin group. Lower rate of coronary lesion progression was also found through follow-up angiography in the cilostazol group (17.4% vs. 23.6%, p = 0.022), especially in nontarget lesions (12.1% vs. 17.6%, p = 0.019). The two groups had the same risk of major bleeding events (0.8% vs. 0.4%, p = 0.364). In the current study, cilostazol is a good substitute for aspirin in patients who have aspirin intolerance but need DAPT after coronary DES implantation in China. However, large-scale randomized controlled trials were still required to further confirm its efficacy and safety.

In-hospital outcome in patients presenting with acute coronary syndrome with left main coronary artery disease: A report from Japanese prospective multicenter percutaneous coronary intervention registry

BackgroundPatients presenting with acute coronary syndrome (ACS) from left main (LM) disease are at a high risk for mortality despite recent advancement in devices and techniques during percutaneous coronary interventions (PCI). We aimed to evaluate patient characteristics, clinical presentations, and key clinical characteristics associated with adverse in-hospital outcomes among ACS patients undergoing LM-PCI. MethodsWe retrospectively identified 280 LM-ACS patients (3.7 %) from 7608 ACS patients in the prospective multicenter Japan Cardiovascular Database-Keio Inter-Hospital Cardiovascular Studies registry from March 2009 to May 2016 and divided them into those with/without PCI/coronary artery bypass grafting. We compared baseline demographics, coronary lesion characteristics, PCI details, and short-term outcomes, including in-hospital mortality and periprocedural complications, between the two groups. ResultsAmong LM-ACS patients, 38.6 % presented with ST elevation myocardial infarction, 29.6 % with cardiogenic shock (CS), and 15.4 % with cardiac arrest. The observed in-hospital mortality rate was 18.9 % with presence of CS [odds ratio (OR): 10.16, 95 % confidence interval (CI): 4.51–22.91, p<0.001] and absence of prior revascularization (de novo patients; OR: 4.31, 95 % CI: 1.43–12.94, p=0.009) was independently associated with higher incidence of in-hospital mortality. Notably, the observed mortality rate was substantially higher among de novo patients than the predicted mortality rate with a contemporary risk model (observed: 25.1 %; predicted: 11.6 %). ConclusionsPrior revascularization act as a protective factor among LM-ACS patients in the contemporary era of PCI. Further studies to detect those at higher risk for LM coronary lesion progression are needed to fully implement these findings into clinical practice.

The History of the WHHL Rabbit, an Animal Model of Familial Hypercholesterolemia (I) - Contribution to the Elucidation of the Pathophysiology of Human Hypercholesterolemia and Coronary Heart Disease -

Animal models that closely resemble both human disease findings and their onset mechanism have contributed to the advancement of biomedical science. The Watanabe heritable hyperlipidemic (WHHL) rabbit and its advanced strains (the coronary atherosclerosis-prone and the myocardial infarction-prone WHHL rabbits) developed at Kobe University (Kobe, Japan), an animal model of human familial hypercholesterolemia, have greatly contributed to the elucidation of the pathophysiology of human lipoprotein metabolism, hypercholesterolemia, atherosclerosis, and coronary heart disease, as described below. 1) The main part of human lipoprotein metabolism has been elucidated, and the low-density lipoprotein (LDL) receptor pathway hypothesis derived from studies using fibroblasts was proven in vivo. 2) Oxidized LDL accumulates in the arterial wall, monocyte adhesion molecules are expressed on arterial endothelial cells, and monocyte-derived macrophages infiltrate the arterial intima, resulting in the formation and progression of atherosclerosis. 3) Coronary lesions differ from aortic lesions in lesion composition. 4) Factors involved in the development of atherosclerosis differ between the coronary arteries and aorta. 5) The rupture of coronary lesions requires secondary mechanical forces, such as spasm, in addition to vulnerable plaques. 6) Specific lipid molecules in the blood have been identified as markers of the progression of coronary lesions. At the end of the breeding of the WHHL rabbit family at Kobe University, this review summarizes the history of the development of the WHHL rabbit family and their contribution to biomedical science.

Pressure overload leads to coronary plaque formation, progression, and myocardial events in ApoE-/- mice.

Hypercholesterolemia and hypertension are two major risk factors for coronary artery diseases, which remain the major cause of mortality in the industrialized world. Current animal models of atherosclerosis do not recapitulate coronary plaque disruption, thrombosis, and myocardial infarction occurring in humans. Recently, we demonstrated that exposure of the heart to high pressure, by transverse aortic constriction (TAC), induced coronary lesions in ApoE-/- mice on chow diet. The aim of this study was to characterize the magnitude and location of coronary lesions in ApoE-/- mice after TAC and to assess the susceptibility of coronary plaque to disruption, leading to myocardial events. Here, we describe a reliable pathological condition in mice characterized by the development of coronary lesions and its progression, leading to myocardial infarction; this model better recapitulates human disease. Following TAC surgery, about 90% of ApoE-/- mice developed coronary lesions, especially in the left anterior descending artery, with 59% of the mice manifesting a different magnitude of LAD stenosis. Myocardial events, identified in 74% of the mice, were mainly due to coronary plaque thrombosis and occlusion. That TAC-induced development and progression of coronary lesions in ApoE-/- mice, leading to myocardial events, represents a potentially novel and important tool to investigate the development of coronary lesions and its sequelae in a setting that better resemble human conditions.

Risk Factors of Intermediate Coronary Lesion Progression

Risk Factors of Intermediate Coronary Lesion Progression

The role of serial carotid intima-media thickness assessment as a surrogate marker of atherosclerosis control in patients with recent myocardial infarction.

IntroductionDespite percutaneous coronary intervention (PCI), patients after their first myocardial infarction (MI) are at high risk of ischemic event recurrence. Therefore, there is a need for objective markers of adequate atherosclerosis control, independent of prescribed pharmacotherapy and patients’ compliance. Such a potential indicator of major adverse cerebral and coronary event (MACCE) risk might be change in carotid intima-media thickness (CIMT), which indicates atherosclerosis growth.AimTo evaluate the potential associations between CIMT changes and the incidence of MACCE and recurrent MI.Material and methodsThe CIMT assessments at baseline and during 2 follow-up visits were performed in 215 patients admitted with MI, in whom PCI was performed for an index lesion, followed by best medical treatment. The incidences of MACCE (cardiovascular death, recurrent MI, ischemic stroke) and new onset angina were recorded prospectively.ResultsThe MACCE were recorded in 65 (30.2%) patients and angina due to coronary lesion progression (CLP) in 27 (12.5%) patients. Although initial CIMT values were similar in patients who suffered MACCE vs. MACCE-free patients (1.43 ±0.40 vs. 1.45 ±0.44 mm; p = 0.486), patients in whom MACCE occurred had greater annual CIMT growth as assessed at the first (0.024 ±0.12 vs. 0.009 ±0.16 mm/year; p < 0.001) and subsequent follow-up visit (0.050 ±0.1 vs. 0.001 ±0.1 mm/year; p < 0.001), in mean 36.5 ±29.3 and 53.3 ±37.1 months, respectively. An optimal cut-off value for annual CIMT change of > 0.003 mm/year (sensitivity: 84.5%, specificity: 49.3%) for MI plus CLP (AUC = 0.673) occurred an independent indicator of MACCE (HR = 3.00; 95% CI: 1.496–6.016), recurrent MI (HR = 4.59, 95% CI: 1.591–13.217), and MI plus CLP (HR = 3.50, 95% CI: 1.759–6.964).ConclusionsAnnual CIMT change might be a potentially valuable marker of atherosclerosis response to post-MI treatment.

Coronary lesion progression as assessed by fractional flow reserve (FFR) and angiography.

The aim of this study was to explore the evolution of coronary lesions which had repeated physiologic evaluation by FFR as an endpoint, describe the clinical significance of longitudinal FFR change (ΔFFR=FFRfollow-up-FFRbaseline) and its correlation with angiographic indices, and identify predictors of FFRfollow-up. A retrospective, single-centre analysis of 414 stenoses (331 patients) with consecutive FFR measurements at least six months apart was performed (median time interval: 24 [17, 37] months). The change in percent diameter stenosis was 2% (-5%, 11%). FFR values at baseline and follow-up were 0.86 (0.82, 0.90) and 0.83 (0.79, 0.90), respectively (<0.0001). The median ΔFFR was -0.007 (-0.028, 0.010) per year. Worsening FFR (ΔFFR <-0.05) was observed in 105 (25%) stenoses, stable FFR (-0.05 ≤ΔFFR ≤0.05) in 276 (67%) and improving FFR (ΔFFR >0.05) in 33 (8%) stenoses. The number of haemodynamically significant stenoses (FFR ≤0.80) was higher at follow-up compared to baseline (33% versus 17%, p<0.0001); ΔFFR correlated weakly with delta diameter stenosis (Δ%DS, ρ=-0.111, p=0.024). In mixed effects repeated measures analysis, only lesion location had an independent correlation with FFR values after adjusting for multiple confounders. In ROC analysis, FFRbaseline values predicted future clinically significant values (c-statistic: 0.736 [95% CI: 0.682-0.783]). FFR values decrease slowly over a two-year follow-up. FFRbaseline, but not angiographic indices, is a predictor of significant functional atherosclerosis progression, predicting which stenoses will require revascularisation.

Morphological features of coronary plaques in WHHLMI rabbits (Oryctolagus cuniculus), an animal model for familial hypercholesterolemia.

In order to examine their suitability for studies on coronary atherosclerosis, we evaluated the features of coronary atherosclerotic plaques in myocardial infarction-prone Watanabe heritable hyperlipidemic (WHHLMI) rabbits, a spontaneous animal model for coronary atherosclerosis and myocardial infarction. Coronary segments of the hearts of 187 WHHLMI rabbits (10–29 months old) were sectioned serially and stained histopathologically and immunohistologically. Progression of coronary lesions was prominent in rabbits that had died suddenly. The degree of coronary lesions of females was higher than that of males. Various types of atherosclerotic lesions were observed in the coronary arteries, such as plaques with a large lipid core covered by a thin fibrous cap, fatty streaks, early and advanced fibroatheromas, fibrous lesions, and advanced lesions with calcium accumulation and the vasa vasorum. In rabbits that had died suddenly, the frequencies of fibroatheromas or advanced lesions were higher than those of rabbits euthanized. Matrix metalloproteinase (MMP)-positive macrophages were detected in gaps among endothelial cells at the plaque surface, beneath the fibrous cap of thin-capped fibroatheromas, and at the bottom of the intimal plaques in which the tunica media was attenuated. Immunohistological results suggest that MMP-positive macrophages are involved in the initiation, progression, and destabilization of coronary plaques, in addition to vascular remodeling, even in WHHLMI rabbits. In conclusion, coronary lesions in WHHLMI rabbits resemble human atherosclerotic lesions, and thus, the WHHLMI rabbit is a suitable animal model for studies on human coronary plaques.

Association of dietary factors with severity of coronary artery disease

Cardiovascular disease has taken epidemic proportions during past decades. Cardiovascular risk factors contribute to progression of coronary lesions, worsening the patient's prognosis. This study was planned to analyze the association of dietary factors with severity of coronary artery disease (CAD) in Indian patients. Three hundred patients with known coronary disease above the age of 25 years were included in this study. Blood samples were collected for biochemical markers. Patients were stratified according to severity of CAD [number of vessel involved-single (SVD), double (DVD), triple (TVD)]. Mean age of the patient was 60.9±12.4 years. Subjects with TVD, DVD, SVD in the study were 52.3%, 25.3% and 22.3% respectively. Patients with TVD had higher body mass index, triglycerides, HOMA-Insulin Resistance, hsCRP and lower high density cholesterol. Diabetes mellitus, hypertension and dyslipidemia were more common in TVD patients. Among macronutrients, patients with TVD had higher intake of carbohydrate and lower intake of protein and dietary fibers. There was no association of total fat intake with CAD, however, intake of palmitic acid was higher among patients with TVD. Intake of vitamins namely niacin, riboflavin, thiamine, B6, and vitamin-C decreased with increase in severity. With increase in severity of CAD, mineral intake (potassium, calcium, magnesium, phosphorus, sulfur, iron, chromium, copper, manganese, and zinc) decreased. Dietary factors are associated with severity of coronary artery disease. Low intake of protein, fiber, vitamins, minerals and high intake of carbohydrate and fat was associated with higher probability of having severe CAD.

Interplay of coronary angiography and intravascular ultrasound in predicting long-term outcomes after heart transplantation

Cardiac allograft vasculopathy (CAV) remains the major cause of late graft-related death after heart transplantation (HT). Identification of patients at risk of cardiovascular events has relevant implications in appropriately guiding resources and intensity of follow-up. In this context, the prognostic relevance of serial coronary imaging long-term after HT is unexplored. Recipients with intravascular ultrasound (IVUS) and coronary angiography performed 1 and 5 years after HT were monitored for subsequent 1 to 10 years to analyze the association of serial coronary imaging with cardiovascular death and major cardiovascular events (MACEs). Included were 131 patients. The MACE incidence was 31.8 per 1,000 patient-years, and cardiovascular mortality was 17.4 per 1,000 patient-years. Progression of coronary lesions detected by angiography and changes in IVUS-defined parameters, including an increase in maximal intimal thickness (MIT) ≥0.35 mm and vascular remodeling, predicted MACE occurrence. However, only MIT change ≥0.35 mm also predicted cardiovascular mortality. Among patients with normal or stable angiography, an MIT change ≥0.35 mm identified those with a significantly higher MACE rate (80 vs 13 events/1,000 patient-years). Worsening metabolic parameters appeared associated with the increasing severity of CAV development. Combined imaging analysis of progression of angiographic lesions and IVUS-detected MIT between 1 and 5 years post-HT allows discriminating patients at high, intermediate, and low risk for adverse long-term cardiovascular outcomes. The metabolic syndrome milieu is confirmed as a key risk factor for long-term CAV progression and adverse prognosis.

A multiscale approach for modeling atherosclerosis progression.

Progression of atherosclerotic process constitutes a serious and quite common condition due to accumulation of fatty materials in the arterial wall, consequently posing serious cardiovascular complications. In this paper, we assemble and analyze a multitude of heterogeneous data in order to model the progression of atherosclerosis (ATS) in coronary vessels. The patient's medical record, biochemical analytes, monocyte information, adhesion molecules, and therapy-related data comprise the input for the subsequent analysis. As indicator of coronary lesion progression, two consecutive coronary computed tomography angiographies have been evaluated in the same patient. To this end, a set of 39 patients is studied using a twofold approach, namely, baseline analysis and temporal analysis. The former approach employs baseline information in order to predict the future state of the patient (in terms of progression of ATS). The latter is based on an approach encompassing dynamic Bayesian networks whereby snapshots of the patient's status over the follow-up are analyzed in order to model the evolvement of ATS, taking into account the temporal dimension of the disease. The quantitative assessment of our work has resulted in 93.3% accuracy for the case of baseline analysis, and 83% overall accuracy for the temporal analysis, in terms of modeling and predicting the evolvement of ATS. It should be noted that the application of the SMOTE algorithm for handling class imbalance and the subsequent evaluation procedure might have introduced an overestimation of the performance metrics, due to the employment of synthesized instances. The most prominent features found to play a substantial role in the progression of the disease are: diabetes, cholesterol and cholesterol/HDL. Among novel markers, the CD11b marker of leukocyte integrin complex is associated with coronary plaque progression.

Insulin resistance predicts progression of de novo atherosclerotic plaques in patients with coronary heart disease: a one-year follow-up study

BackgroundThe aim of our study was to explore and evaluate the relationship between insulin resistance and progression of coronary atherosclerotic plaques. With the great burden coronary heart disease is imposing on individuals, healthcare professionals have already embarked on determining its potential modifiable risk factors in the light of preventive medicine. Insulin resistance has been generally recognized as a novel risk factor based on epidemiological studies; however, few researches have focused on its effect on coronary atherosclerotic plaque progression.MethodsFrom June 7, 2007 to December 30, 2011, 366 patients received their index coronary angiogram and were subsequently found to have coronary atherosclerotic plaques or normal angiograms were consecutively enrolled in the study by the department of cardiology at the Ruijin Hospital, which is affiliated to the Shanghai Jiaotong University School of Medicine. All patients had follow-up angiograms after the 1-year period for evaluating the progression of the coronary lesions. The modified Gensini score was adopted for assessing coronary lesions while the HOMA-IR method was utilized for determining the state of their insulin resistance. Baseline characteristics and laboratory test results were described and the binomial regression analysis was conducted to investigate the relationship between insulin resistance and coronary atherosclerotic plaque progression.ResultsIndex and follow-up Gensini scores were similar between the higher insulin lower insulin resistant groups (9.09 ± 14.33 vs 9.44 ± 12.88, p = 0.813 and 17.21 ± 18.46 vs 14.09 ± 14.18, p =0.358). However the Gensini score assessing coronary lesion progression between both visits was significantly elevated in the higher insulin resistant group (8.13 ± 11.83 versus 4.65 ± 7.58, p = 0.019). Multivariate logistic binomial regression analysis revealed that insulin resistance (HOMA-IR > 3.4583) was an independent predictor for coronary arterial plaque progression (OR = 4.969, p = 0.011). We also divided all the participants into a diabetic (n = 136) and a non-diabetic group (n = 230), and HOMA-IR remained an independent predictor for atherosclerosis plaque progression.ConclusionsInsulin resistance is an independent predictor of atherosclerosis plaque progression in patients with coronary heart disease in both the diabetic and non-diabetic population.