Renal artery revascularization is a controversial treatment strategy for renal artery stenosis: A case series and a brief review of the current literature.

Renal artery stenosis (RAS) may cause secondary hypertension, progressive decline in renal function, and cardiac destabilization syndromes including "flash" pulmonary edema, recurrent congestive heart failure, and cerebro-cardiovascular disease. Atherosclerotic lesions, fibromuscular dysplasia, and vasculitides are the pathophysiological basis of the disease. Common therapeutic pathways for RAS include medical therapy and revascularization with or without stenting. Randomized controlled trials evaluating renal revascularization have not reported any advantages of revascularization over medical therapy alone in terms of renal function improvement or prevention of cardiovascular events. However, mounting clinical experience suggests that the best strategy in RAS management is to identify which patients are most likely to benefit from renal artery stenting and to optimize the safety and durability of the procedure. This review presents 3 cases of patients who have undergone renal revascularization and discusses the available clinical evidence for the identification of RAS patients who will potentially respond well to revascularization.

The importance of characteristics of angina symptoms for the prediction of coronary artery disease in a cohort of stable patients in the modern era.

OBJECTIVE: Angina is an important clinical symptom indicating underlying coronary artery disease (CAD). Its characteristics are important for the diagnosis and risk stratification of patients with CAD. Currently, we aimed to investigate the association of chest pain characteristics with the presence of obstructive CAD in a contemporary cohort of patients undergoing coronary angiography for suspected stable CAD. METHODS: Consecutive patients undergoing coronary angiography for suspected stable CAD (n = 686) in a single university hospital cardiology department were enrolled. Chest pain was classified as typical angina, atypical angina, nonangina chest pain, and lack of symptoms. The presence of significant angiographic CAD was diagnosed by standard coronary angiography. RESULTS: Typical angina symptoms were associated with a higher prevalence of CAD (odds ratio [OR], 3.47, p < 0.001), whereas atypical angina symptoms were associated with a lower prevalence of CAD (OR, 0.49, p = 0.003) than the nonangina symptoms/or asymptomatic status. In multivariate analysis, typical angina symptoms remained an independent predictor of CAD (OR, 2.54, p < 0.001), with a greater predictive accuracy than other clinical risk factors (area under the curve [AUC], 0.715, p < 0.001) and similar to the accuracy of the high-sensitivity C-reactive protein (AUC, 0.712, p < 0.001). In a multivariate model, the combination of all studied factors further improved the predictive accuracy (AUC, 0.81, p < 0.001). CONCLUSION: In a contemporary cohort of patients referred for coronary angiography for stable CAD, the presence of typical angina symptoms was the most important independent predictor of obstructive CAD. The association of atypical angina symptoms with low CAD prevalence compared to nonangina chest pain or absence of significant symptoms probably reflects different management and referral strategies in these groups of patients.

Interleukin-1 genotypes modulate the long-term effect of lipoprotein(a) on cardiovascular events: The Ioannina Study.

BACKGROUND: Lipoprotein(a) [Lp(a)] is a genetic risk factor for cardiovascular disease (CVD), and proinflammatory interleukin-1 (IL-1) genotypes may influence Lp(a)-mediated CVD events. The genotype IL-1(+) is associated with higher rates of inflammation than IL-1(-) genotype. Targeting IL-1ß was recently shown to decrease CVD events independent of low-density lipoprotein-cholesterol levels. OBJECTIVE: The objective of the study is to assess the modulatory effect of IL-1 genotypes on risk mediated by Lp(a) METHODS: We assessed whether IL-1 genotypes modulate the effect of Lp(a) on major adverse cardiovascular events (cardiovascular death, myocardial infarction, and stroke/transient ischemic attack) and angiographically determined coronary artery disease (CAD). IL-1 genotypes and Lp(a) were measured in 603 patients without diabetes mellitus undergoing angiography. Major adverse cardiovascular events and CAD were assessed over a median of 45 months. RESULTS: In multivariable-adjusted analysis, Lp(a) was associated with major adverse cardiovascular events (hazard ratio [HR] [95% confidence interval {CI}]: 2.95 [1.16-7.54], P = .023) and CAD (odds ratio [OR] [95% CI]: 1.84 [1.12-3.03], P = .016) comparing quartile 4 vs quartile 1. In Cox regression analysis, IL-1(+) patients with Lp(a) above the median (>9.2 mg/dL) had a worse event-free cumulative survival (HR [95% CI]: 3.59 [1.07-12.03], P = .039) compared to IL-1(-) patients with Lp(a) below the median. In IL-1(+) patients aged ≤60 years, Lp(a) was also associated with angiographically determined CAD (OR [95% CI]: 2.90 [1.07-7.86], P = .036) comparing quartile 4 vs quartile 1 but not IL-1(-) patients. CONCLUSION: Proinflammatory IL-1(+) genotypes modulate the risk of Lp(a) long-term CVD events and CAD. These data suggest that the dual genetic contributions of elevated Lp(a) levels and IL-1(+) genotypes may identify younger subjects at particularly high risk for CVD events.

Extent of coronary artery disease in patients undergoing angiography for stable or acute coronary syndromes.

BACKGROUND: We aimed to investigate whether the angiographic extent of coronary artery disease (CAD) differs in patients undergoing coronary angiography for stable CAD or acute coronary syndrome (ACS) and identify predictors of CAD extent in these patients. METHODS: We enrolled 584 consecutive patients (463 with stable CAD, 121 with ACS) with angiographically established CAD (≥1 stenosis >25%). The Gensini score was used to assess the extent of coronary atherosclerosis. RESULTS: Stable CAD patients had greater Framingham risk score and greater prevalence of hypertension, hypercholesterolemia, and diabetes (p<0.05 for all). Fasting glucose and systolic and diastolic blood pressure were higher, while high-sensitivity C-reactive protein (hsCRP) levels were lower in patients with stable CAD than in those with ACS (p<0.05 for all). No difference in Gensini score was observed between the two groups (p=0.118), but patients with ACS were more likely to have at least one significant epicardial angiographic lesion (>50% stenosis) (OR 2.0, p=0.022). Higher Gensini score was independently associated with (i) higher hsCRP and glucose levels, hypercholesterolemia, and increased age in stable CAD patients (R2 0.15, p<0001) and (ii) increased age and higher glucose and hsCRP levels in patients with ACS (R2 0.17, p<0001). CONCLUSIONS: Patients undergoing coronary angiography for ACS or stable CAD presented with a similar extent of angiographic CAD, although patients with ACS had a higher prevalence of significant lesions in the presence of a better cardiovascular risk profile and higher inflammation levels. The extent of angiographic CAD in both the groups shared common determinants such as hsCRP, age, and hyperglycemia, but these appeared to explain only a small part of the variation of coronary atherosclerosis.

Large bronchogenic cyst compressing the left atrium.

Bronchogenic cysts are listed among the less common mediastinal tumours and either remain unnoticed and are randomly found or they are manifested with respiratory or thoracic symptoms such as chest pain, dyspnoea, haemoptysis and recurrent thoracic infections. More severe symptoms (e.g. sepsis, compression) are rare. We present a case of a male patient with progressive dyspnoea on exertion attributed to a large bronchogenic cyst.