Increase In Diameter Stenosis Research Articles

Erythropoietin-induced progenitor cell mobilisation in patients with acute ST-segment-elevation myocardial infarction and restenosis

Erythropoietin improves myocardial function and enhances re-endothelialisation. Aim of this study was to analyse progenitor cell mobilisation and restenosis in patients from the Regeneration of Vital Myocardium in ST-Segment Elevation Myocardial Infarction by Erythropoietin (REVIVAL-3) study. Patients with STEMI undergoing percutaneous coronary intervention (PCI) were randomly assigned to Epoetin beta (EPO) (n=68) or placebo (n=70). Drug-eluting stents (DES) were utilised in 93% of patients receiving EPO and in 95% of patients receiving placebo (p=0.83). Serial venous blood samples were drawn; CD133+ progenitor cells were quantified by four-colour flow cytometry and cytokines interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12 and tumour necrosis factor (TNF) alpha were analysed by cytometric bead array. Forty-eight hours after PCI a significant increase in CD133+ progenitor cells was observed in the EPO group. Yet, no differences in plasma cytokines were found. Quantitative coronary angiography after six months revealed an increase in segment diameter stenosis in the EPO group (32 ± 19% vs. 26 ± 14%, p=0.046). However, this increase in neointima generation was not associated with progenitor cell mobilisation. EPO in patients with STEMI treated with PCI is associated with an increase in diameter stenosis that is not associated with circulating progenitor cells.

Association between progression of untreated coronary lesions and in-stent restenosis

Progression of coronary artery disease is only incompletely understood regarding de-novo stenoses as well as in-stent restenoses (ISR) indicative of accelerated atherosclerosis. The objective of the present angiographic study was to prove an association between target lesion ISR and progression of primarily untreated coronary lesions. A total of 179 high-grade native coronary stenoses (mean diameter stenosis 68+/-16 %) of 131 patients were treated by stent implantation. Additional 101 lesions remained untreated because of their moderate to intermediate diameter stenoses (>30 %). Quantitative coronary angiographic analysis was performed 6+/-2 months later to evaluate ISR (diameter stenosis > 50 %), coronary progression (>20 % increase in diameter stenosis) and regression (>20 % decrease), respectively. Angiographic, procedural and clinical characteristics were assessed for a possible association with ISR and/or coronary progression and regression, respectively. ISR was seen in 70 of 179 (39 %) stented target lesions. Presence of diabetes mellitus (p = 0.04) and cumulative duration of inflations (p = 0.01) as procedural determinant were predictive for ISR. Significant progression was found in ten of 101 (10 %) primarily untreated lesions. Progression of previously normal segments or regression were not seen. Progression of native plaques was associated with ISR presence in nine cases and with ISR absence in only one case (p = 0.01). Of note, smoking (p = 0.02) turned out to be predictive for plaque progression, whereas medication and procedural/angiographic parameters were not. The findings of the present pilot study demonstrate target lesion ISR associated with progression of other primarily untreated lesions and thereby suggest that both atherosclerosis types share common systemic pathogenetic mechanisms. With presence of ISR, coronary angiography should also include primarily untreated arteries, especially in case of preexisting plaques.

Hepatic abscess in a diabetic patient

<b>Background:</b> Earlier angiographic studies have suggested that calcium antagonists may prevent the formation of new coronary lesions and the progression of minimal lesions. Conversely, a meta-analysis suggested that these drugs may increase cardiovascular mortality and morbidity in patients with coronary heart disease. <b>Objective:</b> To investigate whether nisoldipine retards the progression of coronary atherosclerosis or reduces the occurrence of clinical events. <b>Design and setting:</b> The NICOLE study (NIsoldipine in COronary artery disease in LEuven) is a single centre, randomised, double blind, placebo controlled trial with coronary angiography at baseline, six months, and three years of follow up. <b>Patients:</b> 826 patients who had undergone successful coronary angioplasty were randomised to nisoldipine 40 mg once daily or placebo. The intention to treat and per protocol population consisted of 819 and 578 patients, respectively. <b>Results:</b> In the per protocol population, 625 of the nisoldipine treated and 655 of the placebo treated patients (NS) showed angiographic progression in at least one coronary arterial segment, defined as an increase in diameter stenosis of ≥ 13%. The average minimum luminal diameter of the non-dilated lesions decreased by 0.163 mm and 0.167 mm in the nisoldipine and placebo groups, respectively (NS). The respective numbers of new lesions detected were 7 and 13 (NS). In the intention to treat population, the rates of death, stroke, and acute myocardial infarction were similar in both treatment groups. However, nisoldipine use was associated with fewer revascularisation procedures and thus the percentage of patients with any clinical event was lower (44.6% <i>v</i> 52.6%, p = 0.02). <b>Conclusions:</b> Nisoldipine has no demonstrable effect on the angiographic progression of coronary atherosclerosis or the risk of major cardiovascular events but its use is associated with fewer revascularisation procedures.

Serum lipoprotein(a) concentrations are related to coronary disease progression without new myocardial infarction.

To examine the association between serum lipoprotein(a) and angiographically assessed coronary artery disease progression without new myocardial infarction. 85 patients with coronary artery disease who underwent serial angiography with an interval of at least two years were studied. Progression of coronary artery disease was defined as an increase in diameter stenosis of 15% or more. Vessels on which angioplasty had been performed were excluded from the analysis. The patients were classified into two groups: a progression group without new myocardial infarction (n = 48) and non-progression group (n = 37). Risk factors including lipoprotein(a) were evaluated to see how they were related to progression without myocardial infarction. There were no differences between the two groups in the following factors: age, gender, the time interval between the angiographic studies, the distribution of the analysed coronary arteries, and history of well established coronary risk factors. Univariate analysis showed that serum lipoprotein(a) (P = 0.0002), cigarette smoking between the studies (P = 0.002), serum high density lipoprotein (P = 0.003), and serum low density lipoprotein (P = 0.01) were related to progression without myocardial infarction. Multivariate analysis selected two independent factors for progression without myocardial infarction: serum lipoprotein(a) (P = 0.003) and serum high density lipoprotein (P = 0.03). Serum lipoprotein(a) concentrations are closely related to the progression of coronary artery disease without new myocardial infarction. Lipoprotein(a) lowering treatment may be needed to prevent disease progression in patients with coronary artery disease and high serum lipoprotein(a).

Differential progression of complex and smooth stenoses within the same coronary tree in men with stable coronary artery disease

We sought to compare the evolution of complex and smooth stenoses within the same coronary tree in patients with stable coronary artery disease. Progression of coronary stenosis has prognostic significance and may be influenced by local and systemic factors. Stenosis morphology is a determinant of disease progression, but no previous study has systematically assessed progression of complex and smooth stenoses within the same patient. We studied 50 men with stable angina who 1) had one complex coronary stenosis and one smooth stenosis in different noninfarct-related coronary vessels at initial coronary angiography, and 2) had a second angiogram after a median interval of 9 months (range 3 to 24). Patients with lesions > or = 10 mm long, at a major branching point or with > 85% diameter reduction were not included. Coronary lesions were measured quantitatively from comparable end-diastolic frames. Stenosis morphology was determined qualitatively by two independent observers. All patients remained in stable condition during follow-up. Progression, defined as an increase in diameter stenosis by > or = 15% was seen in only eight complex stenosis (16%) but in no smooth lesions (p < 0.01). The severity of complex stenoses changed more than that of corresponding smooth stenoses (mean +/- 1 SD 5.8 +/- 13% vs. -0.06 +/- 6%, p < 0.01). On average, the annual rate of growth was 11.4 +/- 28% and 1.5 +/- 14% for complex and smooth lesions, respectively (p < 0.01). Few coronary stenoses progress rapidly in stable angina. Complex and smooth coronary stenoses progress at different rates within the same coronary tree. complex stenosis morphology itself is an important determinant of progression of stenosis in patients with apparently clinically stable coronary artery disease.

Early decrease in minimal luminal diameter after successful percutaneous transluminal coronary angioplasty predicts late restenosis

Eighty-eight patients underwent serial coronary arteriography before, immediately after, 24 hours after and 7 ± 2 months after successful percutaneous transluminal coronary angioplasty (PTCA) of 102 lesions. Severity of coronary obstruction was measured using quantitative digital angiography. Three groups of lesions were defined when comparing angiograms recorded immediately after and 24 hours after PTCA: group I — lesions with either no change or <-10% increase in arterial diameter stenosis after PTCA (n = 71); group II—lesions with >10% increase in diameter stenosis after PTCA (n = 19); and group III — patients with total occlusion (n = 12). There were no significant differences in the severity of stenosis before or immediately after PTCA among the 3 groups of lesions. Twenty-four hours after PTCA the diameter stenosis was 14.2 ± 6.3% in group I, 34.7 ± 8.1% in group II and 100 in group III (p < 0.0001). At 7.1 ± 2 months after PTCA the diameter stenosis was 21.2 ± 16.8% in group I, 61.3 ± 1.1% in group II, and 98.5 ± 1.3% in group III (p < 0.0001). Restenosis (≥ 50% stenosis diameter) at follow-up per lesion was significantly greater in group II than in group I (73.6 vs 9.8%) (p < 0.0001). Thus, early angiographic study after successful PTCA stratifies lesions into angiographic subsets with low (group I) and high (group II) risk of coronary restenosis.

Prognostic significance of progression of coronary atherosclerosis.

Angiographic progression of coronary atherosclerosis is frequently observed in clinical practice and is used as an end point in clinical trials; however, its prognostic significance is unclear. Progression defined as an increase in diameter stenosis by > or = 15% of at least one coronary lesion was seen in 141 (42%) of 335 patients who underwent repeat coronary arteriography after a 2-year interval as part of clinical trial. Coronary lesions were measured quantitatively from comparable end-diastolic frames selected by a radiologist viewing each pair of films together. During a mean follow-up of 44 +/- 10 months after the second arteriogram, cardiac death occurred in 19 patients (5.7%), cardiac death or nonfatal infarction was seen in 40 cases (11.9%), and 90 patients (26.9%) underwent coronary revascularization. At least one end point event occurred in 112 of the 335 patients. Sixteen of the 19 cardiac deaths were in progressors, a relative risk of 7.3 (95% CI, 2.2-24.7; p < 0.001). The relative risk of cardiac death or nonfatal infarction for progressors was 2.3 (1.3-4.2, p = 0.009) and of any cardiac event was 1.7 (1.3-2.3, p < 0.001). A stepwise multivariable Cox regression model of time to event was used to assess the relative contribution of progression as a predictor of coronary events. Low ejection fraction (p = 0.001), progression (p = 0.001), and hypertension (p = 0.011) were retained as predictors of cardiac death. Angina and the number of diseased vessels were the strongest predictors of revascularization. Coronary progression is a strong, independent predictor of future coronary events, particularly cardiac death, and its use as a surrogate end point in clinical trials is justified.