The Postoperative Paradoxical Septum (POPS): A Comprehensive Review on Physio-Pathological Mechanisms.

The interventricular septum (IVS) is a core myocardial structure involved in biventricular coupling and performance. Physiologically, during systole, it moves symmetrically toward the center of the left ventricle (LV) and opposite during diastole. Several pathological conditions produce a reversal or paradoxical septal motion, such as after uncomplicated cardiac surgery (CS). The postoperative paradoxical septum (POPS) was observed in a high rate of cases, representing a unicum in the panorama of paradoxical septa as it does not induce significant ventricular morpho-functional alterations nor negative clinical impact. Although it was previously considered a postoperative event, evidence suggests that it might also appear during surgery and gradually resolve over time. The mechanism behind this phenomenon is still debated. In this article, we will provide a comprehensive review of the various theories generated over the past fifty years to explain its pathological basis. Finally, we will attempt to give a heuristic interpretation of the biventricular postoperative motion pattern based on the switch of the ventricular anchor points.

Advances in Multimodality Cardiovascular Imaging in the Diagnosis of Heart Failure With Preserved Ejection Fraction.

Heart failure with preserved ejection fraction (HFpEF) is a syndrome defined by the presence of heart failure symptoms and increased levels of circulating natriuretic peptide (NP) in patients with preserved left ventricular ejection fraction and various degrees of diastolic dysfunction (DD). HFpEF is a complex condition that encompasses a wide range of different etiologies. Cardiovascular imaging plays a pivotal role in diagnosing HFpEF, in identifying specific underlying etiologies, in prognostic stratification, and in therapeutic individualization. Echocardiography is the first line imaging modality with its wide availability; it has high spatial and temporal resolution and can reliably assess systolic and diastolic function. Cardiovascular magnetic resonance (CMR) is the gold standard for cardiac morphology and function assessment, and has superior contrast resolution to look in depth into tissue changes and help to identify specific HFpEF etiologies. Differently, the most important role of nuclear imaging [i.e., planar scintigraphy and/or single photon emission CT (SPECT)] consists in the screening and diagnosis of cardiac transthyretin amyloidosis (ATTR) in patients with HFpEF. Cardiac CT can accurately evaluate coronary artery disease both from an anatomical and functional point of view, but tissue characterization methods have also been developed. The aim of this review is to critically summarize the current uses and future perspectives of echocardiography, nuclear imaging, CT, and CMR in patients with HFpEF.

Combined use of high-sensitivity C-reactive protein and N-terminal pro-B-type natriuretic peptide for risk stratification of vascular surgery patients.

BACKGROUND: We sought to assess whether high-sensitivity C-reactive protein (hs-CRP) and pro-B-type natriuretic peptide (NT-proBNP) improve risk prediction when added to an established predictive tool and develop a point-based risk score. METHODS: Four hundred eleven vascular surgery patients were enrolled. The primary outcome was a composite of death, acute coronary syndromes, pulmonary edema within 30 days of surgery, and postoperative troponin-I elevation. The risk score was developed from a logistic regression model by using an integer-based scoring system. RESULTS: The rate of the primary outcome was 18%. Adding both hs-CRP and NT-proBNP to the Revised Cardiac Risk Index led to an increase in C statistic from 0.670 to 0.774. The net reclassification improvement was 0.210 (P = 0.004) and the integrated discrimination improvement was 0.112 (P = 0.0001). In the multivariable regression analysis used to develop the risk score, insulin therapy for diabetes (odds ratio [OR]: 2.8; P = 0.003), open surgery (OR: 1.95; P = 0.027), fibrinogen >377 mg/dL (OR: 2.83; P = 0.001), hs-CRP >3.2 mg/L (OR: 3.85; P < 0.0001), and NT-proBNP >221 ng/L (OR: 4.05; P < 0.0001) were associated with the primary outcome. There was no statistical evidence of overfit. The C index was 0.82 and the Hosmer-Lemeshow statistic was 1.61 (P = 0.0447). The observed and predicted rates of the primary outcome across quartiles of risk score were highly correlated. CONCLUSIONS: Hs-CRP and NT-proBNP substantially improve risk prediction when added to an established predictive tool. The biochemical marker-based risk score may be useful for accurately risk-stratifying vascular surgery patients; nonetheless, further validation studies on external datasets are needed before it can be used in clinical practice.

High-sensitivity C-reactive protein predicts cardiovascular events and myocardial damage after vascular surgery.

OBJECTIVE: To assess the association of high-sensitivity C-reactive protein (hsCRP) to adverse cardiovascular events and perioperative myocardial damage in patients after elective vascular surgery. METHODS: This was a prospective observational study in a tertiary-care teaching hospital, with 239 patients undergoing elective vascular surgery. The receiver-operating characteristic (ROC) curve was calculated to assess the optimal cut-off value of hsCRP. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Multiple logistic regression analysis was used to identify the predictors of the primary outcome. The primary outcome was a composite of periprocedural myocardial damage, defined as cardiac troponin I (cTn-I) elevation above the decision limit of 0.15 µg/L, death, acute coronary syndrome, stroke, acute heart failure, or intrastent thrombosis within 30 days of surgery. RESULTS: On ROC analysis, the optimal cut-off value of hsCRP was 3.2 mg/L. The primary outcome occurred in 48 patients (20.1%). On univariate analysis, smoking (P = .009), known hypercholesterolemia (P = .01), previous ischemic heart disease (P = .0003), open surgery (P = .03), and hsCRP levels (P < .0001) were associated with the primary outcome. On multiple logistic regression analysis, only hsCRP was independently associated with the primary outcome. The unadjusted and adjusted ORs for the primary outcome among patients with hsCRP levels >3.2 mg/L were 7.5 (CI, 3.7-15.2; P < .0001) and 4.6 (CI, 2.1-9.9; P = .0001), respectively. CONCLUSION: Our data suggest that higher levels of hsCRP are independently associated with an increased risk of perioperative myocardial damage and early adverse cardiovascular events in patients undergoing elective vascular surgery. This may have implications for risk stratification and therapeutic approach.

Induction of functional neovascularization by combined VEGF and angiopoietin-1 gene transfer using AAV vectors.

Vectors based on the adeno-associated virus (AAV) deliver therapeutic genes to muscle and heart at high efficiency and maintain transgene expression for long periods of time. Here we report about the synergistic effect on blood vessel formation of AAV vectors expressing the 165 aa isoform of vascular endothelial growth factor (VEGF165), a powerful activator of endothelial cells, and of angiopoietin-1 (Ang-1), which is required for vessel maturation. High titer AAV-VEGF165 and AAV-Ang-1 vector preparations were injected either alone or in combination in the normoperfused tibialis anterior muscle of rats. Long term expression of VEGF165 determined massive cellular infiltration of the muscle tissues over time, with the formation of a large set of new vessels. Strikingly, some of the cells infiltrating the treated muscles were found positive for markers of activated endothelial precursors (VEGFR-2/KDR and Tie-2) and for c-kit, an antigen expressed by pluripotent bone marrow stem cells. Expression of VEGF165 eventually resulted in the formation of structured vessels surrounded by a layer of smooth muscle cells. Presence of these arteriolae correlated with significantly increased blood perfusion in the injected areas. Co-expression of VEGF165 with angiopoietin-1-which did not display angiogenic effect per se-remarkably reduced leakage of vessels produced by VEGF165 alone.