Systematic review and meta-analysis on coronary calcifications in COVID-19.

Chest CT is valuable to detect alternative diagnoses/complications of COVID-19, while its role for prognostication requires further investigation. Non-pulmonary radiological findings such as cardiovascular calcifications could increase the predictivity of clinical outcomes of COVID-19 patients beyond pulmonary involvement. Several observational studies have reported mixed results on the role of coronary calcifications in COVID-19 patients as a predictor of hospitalization, ventilatory support, and mortality. The purpose of the study is to systematically review the available evidence on the predictive role of cardiovascular calcifications in SARS-CoV2 disease. The meta-analysis confirms the prognostic significance of coronary calcifications on hospital mortality, and coronary calcifications (CAC ≠ 0) were associated with an OR for mortality of 2.19 (95% CI 1.36-3.52). CAC was neutral on respiratory outcomes, but it was associated with an increased trend of cardiovascular events. Coronary calcium appears as a promising biomarker imaging even in short-term outcomes (MACEs, hospital mortality) in a non-cardiovascular disease such as Sars-CoV2 infection. Further large studies are needed to confirm promising results of this imaging biomarker in non-cardiovascular disease.

Identification of differentially expressed genes in coronary atherosclerotic plaques from patients with stable or unstable angina by cDNA array analysis.

The composition of atherosclerotic plaques is a crucial factor in determining rupture, thrombosis and clinical events. In this study, we analyzed gene expression in coronary plaques from patients with stable or unstable angina using gene arrays. Total RNA was extracted from eight plaques collected by therapeutic directional coronary atherectomy. cDNA probes, generated by amplification, were hybridized to nylon arrays containing 482 genes. Here we report the results for the inflammation, adhesion and hemostasis subsets. Many genes not previously associated with atherosclerosis, such as the lymphocyte adhesion molecule MadCAM, were expressed in the plaques. anova analysis showed higher tissue factor (TF) expression in unstable angina samples. Five genes were expressed at lower levels in unstable angina samples: anticoagulant protein S, cyclooxygenase (COX)-1, interleukin (IL)-7 and chemokines monocyte chemotactic protein (MCP)-1 and -2. Gene arrays provide a new approach to study plaque composition and identify candidate markers of plaque instability.

Perioperative myocardial infarction in noncardiac surgery: the diagnostic and prognostic role of cardiac troponins.

Despite the number of technologies used, the diagnosis of perioperative myocardial infarction is still a challenge. Studies conducted in surgical series have demonstrated that cardiac troponins (cTns) have both a superior diagnostic sensitivity and specificity, compared with other traditional techniques, and an independent power to predict short- and long-term prognosis. Nevertheless, some points need to be clarified. They include the usefulness of cTns in patients with end-stage renal failure; the standardization of the cTns cut-off for the diagnosis of myocardial injury; the timing of postoperative blood samplings; the cost-effectiveness of a screening in asymptomatic patients; and the possible therapeutic strategies.

Thrombogenic potential of human coronary atherosclerotic plaques.

Higher levels of tissue factor (the initiator of blood coagulation) have been found in coronary atherosclerotic plaques of patients with unstable coronary artery disease, but it is not established whether they are associated with a different thrombotic response to in vivo plaque rupture. In 40 patients undergoing directional coronary atherectomy, prothrombin fragment 1 + 2, a marker of thrombin generation, was measured in intracoronary blood samples obtained proximally and distally to the coronary atherosclerotic plaque before and after the procedure. Before the procedure, plasma prothrombin fragment 1 + 2 levels were significantly increased across the lesion in patients with unstable, but not in those with stable, coronary disease (unstable, median increase, 0.37 nM; range, -0.35-1.16 nM) (stable, median increase, -0.065 nM; range, -0.58-1.06 nM) (P =.0021). After plaque removal, an increase in prothrombin fragment 1 + 2 across the lesion was observed only in patients with unstable coronary disease (unstable, median increase, 0.25 nM; range, -1.04-4.9 nM) (stable, 0.01 nM; range, -0.48-3.59 nM) (P =.036)]. There was a correlation between the tissue factor content of the plaque and the increase in thrombin generation across the lesion (rho = 0.33; P =.038). The higher tissue factor content found in plaques obtained from patients with unstable coronary disease was associated with a local increase in thrombin generation, thus suggesting a link with the in vivo thrombogenicity of the plaque.

Five-minute recording of heart rate variability in severe chronic heart failure: correlates with right ventricular function and prognostic implications.

BACKGROUND: In advanced chronic heart failure (CHF), correlation between heart rate variability (HRV) and parameters of disease severity is still unclear. A reduced HRV has been related to left but not to right ventricular function parameters. Moreover, the prognostic role of spectral measures is not fully defined. We sought to assess HRV by using a short electrocardiographic recording in ambulatory patients with severe CHF to investigate the relation of HRV with clinical neurohormonal and hemodynamic parameters and to determine its predictive prognostic power. METHODS AND RESULTS: HRV was obtained from 5-minute electrocardiographic recordings in 75 ambulatory patients with CHF referred for heart transplantation screening. Standard frequency-domain parameters (total power, low-frequency power, and high-frequency power) were calculated. Prognostic value of these autonomic markers and their correlation with clinical and instrumental parameters were also assessed. A low low-frequency/high-frequency ratio was an independent predictor of cardiac events (P =.015). No correlation was found between New York Heart Association class and HRV, whereas significant correlations were identified between norepinephrine plasma levels, several hemodynamic parameters, and spectral measures (P < or =.03). A reduced HRV, particularly a low-frequency power reduction (P =.000), was highly related to indexes of right ventricular dysfunction. CONCLUSIONS: The current data indicate that spectral analysis of HRV, calculated from short electrocardiographic recordings, may represent a simple but effective means contributing to risk stratification of patients with severe CHF. Autonomic information obtained from this analysis suggests that right ventricular dysfunction may be a critical element determining autonomic imbalance in patients with severe CHF.

Tissue factor in human coronary atherosclerotic plaques.

The rupture or fissuring of a coronary atherosclerotic plaque and subsequent thrombosis is considered the key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque disruption frequently occurs during the evolution of atherosclerosis, only a minority of ruptured plaques develop thrombosis. The content and procoagulant activity of tissue factor in human coronary atherosclerotic plaques varies widely, and different studies confirm that it is higher in the plaques extracted from patients with unstable angina, myocardial infarction or histologic/angiographic evidence of coronary thrombosis than in those taken from patients with stable angina or uncomplicated coronary lesions. Variations in tissue factor content and activity may be responsible for the different thrombotic responses to human coronary atherosclerotic plaque rupture.

Antithrombotic therapy of unstable angina and non-Q-wave myocardial infarction.

Unstable angina and non-Q-wave myocardial infarction still represent an unsolved problem for clinicians, owing to their unpredictable evolution and high incidence of coronary events in the follow-up. Traditional antithrombotic agents, unfractionated heparin and aspirin, have been proved to be highly effective, but show some important limitations. New potent antithrombotic therapy have been studied to improve their efficacy, with encouraging results. Among these drugs, low molecular weight heparins (for subcutaneous administration) and inhibitors of platelet glycoprotein receptor IIb/IIIa (for intravenous, and possibly oral, administration) are the most promising and are now under extensive investigation.

[Coronary lesion with an aneurysm: their correction via angioplasty and the implantation of a coated stent]. / Lesione coronarica con aneurisma: correzione mediante angioplastica ed impianto di stent ricoperto.

We describe the good angiographic results obtained using a new polymeric prosthesis combining a stent with expandable polytetrafluoroethylene (PTFE) graft material in the treatment of proximal left descending coronary artery stenosis complicated by the presence of a coronary aneurysm.

Ten-year experience with endomyocardial biopsy in myocarditis presenting with congestive heart failure: frequency, pathologic characteristics, treatment and follow-up.

The present study summarizes our ten-year (1985-1995) experience with endomyocardial biopsy (EMB) in patients with idiopathic congestive heart failure (CHF), with specific reference to frequency of myocarditis, treatment policy, relative benefits, and follow-up. Of the 601 patients who constituted our series, 38 were clinically suspected of having myocarditis on the bases of a very recent onset of congestive heart failure and/or of arrhythmias and/or of conduction disturbances, and of a close-to-recent history of flu-like febrile illness. Corresponding EMBs showed myocarditis in 16 of the 38 cases (42.1%). A further 10 EMBs, from patients with a recent onset of congestive heart failure without prior infection episodes, showed myocarditis. Therefore, biopsy-proven myocarditis occurred in 26 of the 601 patients (4.3%). Of the 26 cases, 21 were lymphocytic, 1 was necrotizing granulomatous, 1 was eosinophilic and occurred in a patient who later developed overt zoonosis, 1 had some giant cells within endocardial inflammatory infiltrates, and 2 were borderline forms. In active myocarditis, inflammatory cells mostly constituted of T-lymphocytes (CD45RO+) with sparse macrophages (CD68+) and a few B cells (CD20+). B-lymphocytes and macrophages, along with activated T-lymphocytes, all expressed MHC class II HLA DR molecules, which were also expressed "de novo" by activated endothelial calls of capillaries and of small intramural vessels. HLA DR revealed itself as a very useful marker for the detection of activated inflammatory and endothelial cells. We also noted an increase in the number of perivascular and interstitial mast cells. Ultrastructural study was helpful for the characterization of myocyte damage and of interactions between inflammatory cells and myocytes. In 4 cases (1 of whom was later revealed as HIV positive, and subsequently died of AIDS), we found microreticulotubular structures in endothelial cells of small vessel and capillaries; in 7 cases, there were myocyte changes similar to those described in polymyositis; in 1 case, we observed subplasmalemmal buddings, but no viral particles; in 6 cases, there was extensive myocyte damage with myofibrillar lysis and focal adipous metaplasia; the remaining 6 cases showed myocyte damage of differing extent and severity; in the borderline forms, such damage coexisted with interstitial fibrosis. One of the 21 lymphocytic myocardites was not treated because during hospital screening the patient proved to be HIV positive; of the remaining 20 active myocardites, 11 were treated with a 6-month tapered steroid and azathioprine protocol (one was treated for 24 months), while 9 were not treated. The corresponding follow-up was: 6 deaths (congestive heart failure), 2 cardiac transplants and 3 survivals (1 with pace-maker) in the treated group, and 3 deaths (2 of congestive heart failure and 1 of sudden death), 1 cardiac transplant and 5 survivals (1 on the waiting list for transplantation) in the non-treated group. One of the 2 patients with borderline myocarditis died of congestive heart failure, and 1 is alive. Of the 22 patients with clinical diagnosis of myocarditis and negative biopsy, 7 died of congestive heart failure (2 on the waiting list for transplantation), 4 underwent cardiac transplantation, and 11 are alive (1 is awaiting transplantation). Of the 20 patients currently alive, 1 was originally in NYHA class III, 15 were in class II and 4 were in class I. Of the 20 overall patients who died, 12 were originally in NYHA class IV, 6 in class III, 2 in class II; of the 8 patients who underwent transplantation, 6 were originally in NYHA class IV and 2 in class III. Our overall experience shows that the frequency of myocarditis diagnosed according to Dallas criteria is high in patients with clinical diagnosis of myocarditis, while it is extremely low in dilated cardiomyopathy patients. This finding suggests that, although non-specific, recent onset of symptoms and prior febrile infe

Comparison of coronary lesions obtained by directional coronary atherectomy in unstable angina, stable angina, and restenosis after either atherectomy or angioplasty.

The present study investigated the incidence of the histopathologic lesions and of growth factor expression in a consecutive series of directional coronary atherectomy (DCA) samples from 40 unstable angina pectoris patients without prior acute myocardial infarction and compared the findings with those obtained in DCA samples from 18 patients with stable angina without previous infarction and 18 patients with restenosis. We investigated coronary thrombosis, neointimal hyperplasia, and inflammation. For unstable angina, we correlated the angiographic Ambrose plaque subtypes with the histopathologic findings. The immunophenotype of plaque cells and the growth factor expression were assessed with specific antibodies for cell characterization and for the expression of basic fibroblast and platelet-derived AA and AB growth factors and receptors. The incidence of coronary thrombosis was 35% in patients with unstable angina, 17% in those with stable angina, and 11% in patients with restenosis. Neointimal hyperplasia was found in 38% of unstable angina cases, in 17% of stable angina cases, and in 83% of restenosis cases. Inflammation without thrombus or accelerated progression occurred in 20% of unstable angina and 6% of stable angina samples. In 52% of unstable angina cases, inflammation coexisted with thrombosis and/or neointimal hyperplasia. In the unstable angina group, 71% of the plaques with thrombus had a corresponding angiographic pattern of complicated lesions. The growth factor expression, reported as percentage of cells immunostaining with different growth factor antibodies, was highest in restenosis, followed by unstable angina and stable angina lesions.(ABSTRACT TRUNCATED AT 250 WORDS)