584 research outputs found
Skeletal features in patient affected by maxillary canine impaction
Objective: To analyze the skeletal features of patients with maxillary canine impaction.
Material and Methods: The complete pre-treatment records of 1674 orthodontic patients were examined. From the
subjects with maxillary impacted canine 12 patients were excluded , remaining 108. The subjects with maxillary
impacted canine were divided into two study groups: a palatally displaced canine group (PDCG) (77 patients) and
a buccally displaced canine group (BDCG) (31 patients). The values of the skeletal features measured on the lateral
cephalometric radiograph were compared with a control group (CG) of 121 subjects randomly selected from the
initial sample without maxillary canine impaction. The statistical analysis of the difference between the study
groups and the CG was tested using X2 test and Fisher's exact test. The level of significance was set at P <=0.05.
Results: The CG was characterized by increased values of A point-Nasion-B point angle (ANB) and by a retropositioned or smaller lower jaw. PDCG patients showed normal skeletal features compared to the CG, presenting
mainly I class and lower rank of II and III sagittal skeletal features. PDCG subjects presented also normal values
of the Steiner vertical skeletal relationship angles with normal facial divergence compared to the CG. PDCG cases
were also characterized by horizontal and prognathic growth. BDCG did not present significant differences in
skeletal features compared to the CG, except for an increased ANB.
Conclusions: Palatally displaced canine (PDC) was frequently the only orthodontic problem of patients and was not
associated whit altered skeletal features. The frequent absence of malocclusion in PDC patients explains the delayed
identification of this problem. BDCG patients did not present significant differences in skeletal features with respect to the orthodontic population. The presence of both buccally displaced canine (BDC) and malocclusion makes the patient with BDC both aware of the need for, and motivated to undergo, orthodontic treatment
SARS-CoV-2 Related Myocarditis. What We Know So Far
A minority of patients with severe acute respiratory syndrome coronavirus 2 (COVID-19) develop cardiovascular complications, such as acute cardiac lesions with elevated troponins, de novo systolic heart failure, pericardial effusion and, rarely, acute myocarditis. The prevalence of COVID-19-related myocarditis ranges from 10 to 105 cases per 100,000 COVID-19-infected individuals, with a male predominance (58%) and a median age of 50 years. The etiopathogenetic mechanism is currently unclear, but may involve direct virus-mediated damage or an exaggerated immune response to the virus. Mortality is high, as fulminant myocarditis (FM) develops very often in the form of cardiogenic shock and ventricular arrhythmias. Hence, medical therapy with ACE inhibitors and beta-blockers may not always be sufficient, in which case inotropic and immunosuppressive drugs, most commonly corticosteroids, may be necessary. In this review we analyze the current data on COVID-19 myocarditis, management strategies and therapy, with a brief description of COVID-19 vaccine-associated myocarditis to help clinicians dealing with this peculiar form of myocarditis
Diabetes does not impact the diagnostic performance of contrast-based fractional flow reserve: insights from the CONTRAST study
Background: Adenosine-free coronary pressure wire metrics have been proposed to test the functional significance
of coronary artery lesions, but it is unexplored whether their diagnostic performance might be altered in patients with
diabetes.
Methods: We performed a post-hoc analysis of the CONTRAST study, which prospectively enrolled an international
cohort of patients undergoing routine fractional flow reserve (FFR) assessment for standard indications. Paired,
repeated measurements of all physiology metrics (Pd/Pa, iFR, contrast-based FFR, and FFR) were made. A central core
laboratory analyzed blinded pressure tracings in a standardized fashion.
Results: Of 763 subjects enrolled at 12 international centers, 219 (29%) had diabetes. The two groups were wellbalanced
for age, clinical presentation (stable or unstable), coronary vessel studied, volume and type of intracoronary
contrast, and volume of intracoronary adenosine. A binary threshold of cFFR ≤ 0.83 produced an accuracy superior
to both Pd/Pa and iFR when compared with FFR ≤ 0.80 in the absence of significant interaction with diabetes status;
indeed, accuracy in subgroups of patients with or without diabetes was similar for cFFR (86.7 vs 85.4% respectively;
p = 0.76), iFR (84.2 vs 80.0%, p = 0.29) and Pd/Pa (81.3 vs 78.9%, p = 0.55). There was no significant heterogeneity
between patients with or without diabetes in terms of sensitivity and specificity of all metrics. The area under
the receiver operating characteristic (ROC) curve was largest for cFFR compared with Pd/Pa and iFR which were
equivalent (cFFR 0.961 and 0.928; Pd/Pa 0.916 and 0.870; iFR 0.911 and 0.861 in diabetic and non-diabetic patients
respectively).
Conclusions: cFFR provides superior diagnostic performance compared with Pd/Pa or iFR for predicting FFR irrespective
of diabetes (clinicaltrials.gov identifier NCT02184117)
Prevalence of Coronary Microvascular Disease and Coronary Vasospasm in Patients With Nonobstructive Coronary Artery Disease: Systematic Review and Meta-Analysis
Background A relevant proportion of patients with suspected coronary artery disease undergo invasive coronary angiography showing normal or nonobstructive coronary arteries. However, the prevalence of coronary microvascular disease (CMD) and coronary spasm in patients with nonobstructive coronary artery disease remains to be determined. The objective of this study was to determine the prevalence of coronary CMD and coronary vasospastic angina in patients with no obstructive coronary artery disease. Methods and Results A systematic review and meta-analysis of studies assessing the prevalence of CMD and vasospastic angina in patients with no obstructive coronary artery disease was performed. Random-effects models were used to determine the prevalence of these 2 disease entities. Fifty-six studies comprising 14 427 patients were included. The pooled prevalence of CMD was 0.41 (95% CI, 0.36-0.47), epicardial vasospasm 0.40 (95% CI, 0.34-0.46) and microvascular spasm 24% (95% CI, 0.21-0.28). The prevalence of combined CMD and vasospastic angina was 0.23 (95% CI, 0.17-0.31). Female patients had a higher risk of presenting with CMD compared with male patients (risk ratio, 1.45 [95% CI, 1.11-1.90]). CMD prevalence was similar when assessed using noninvasive or invasive diagnostic methods. Conclusions In patients with no obstructive coronary artery disease, approximately half of the cases were reported to have CMD and/or coronary spasm. CMD was more prevalent among female patients. Greater awareness among physicians of ischemia with no obstructive coronary arteries is urgently needed for accurate diagnosis and patient-tailored management.
Keywords: angina with nonobstructive coronary artery disease; ischemia with no obstructive coronary artery disease; vasospastic angina
Intracoronary EnalaPrilat to Reduce MICROvascular Damage During Percutaneous Coronary Intervention (ProMicro) study.
Intracoronary angiotensin-converting enzyme inhibitors have been shown to relieve myocardial ischemia in stable patients and to improve epicardial flow in patients with ST-segment elevation myocardial infarction. Yet, it is
still unclear whether these effects are mediated by a modulation of the coronary microcirculation.
Methods We randomly assigned 40 patients to receive either an intracoronary bolus of enalaprilat (50 g) or placebo before elective PCI. The index of microvascular resistance was measured at baseline, 10 minutes after study drug
administration, and after PCI. High-sensitivity cardiac troponin T was measured as a marker of myocardial injury.
Results Infusion of enalaprilat resulted in a significant reduction in index of microvascular resistance (27 11 at baseline vs. 19 9 after drug vs. 15 8 after PCI), whereas a significant post-procedural increase in index of microvascular resistance levels was observed in the placebo group (24 15 at baseline vs. 24 15 after drug vs.
33 19 after PCI). Index of microvascular resistance levels after PCI were significantly lower in the enalaprilat
group (p 0.001). Patients pre-treated with enalaprilat also showed lower peak values (mean: 21.7 ng/ml,
range: 8.2 to 34.8 ng/ml vs. mean: 32.3 ng/ml, range: 12.6 to 65.2 ng/ml, p 0.048) and peri-procedural increases of high-sensitivity cardiac troponin T (mean: 9.9 ng/ml, range: 2.7 to 19.0 ng/ml vs. mean: 26.6 ng/ml,
range: 6.3 to 60.5 ng/ml, p 0.025).
Conclusions Intracoronary enalaprilat improves coronary microvascular function and protects myocardium from procedurerelated injury in patients with coronary artery disease undergoing PCI. Larger studies are warranted to investigate whether these effects of enalaprilat could result into a significant clinical benefit. (J Am Coll Cardiol
2013;61:615–21) © 2013 by the American College of Cardiology Foundatio
Deferral of Coronary Revascularization in Patients With Reduced Ejection Fraction Based on Physiological Assessment: Impact on Long-Term Survival
Background Deferring revascularization in patients with nonsignificant stenoses based on fractional flow reserve (FFR) is associated with favorable clinical outcomes up to 15 years. Whether this holds true in patients with reduced left ventricular ejection fraction is unclear. We aimed to investigate whether FFR provides adjunctive clinical benefit compared with coronary angiography in deferring revascularization of patients with intermediate coronary stenoses and reduced left ventricular ejection fraction. Methods and Results Consecutive patients with reduced left ventricular ejection fraction (≤50%) undergoing coronary angiography between 2002 and 2010 were screened. We included patients with at least 1 intermediate coronary stenosis (diameter stenosis ≥40%) in whom revascularization was deferred based either on angiography plus FFR (FFR guided) or angiography alone (angiography guided). The primary end point was the cumulative incidence of all-cause death at 10 years. The secondary end point (incidence of major adverse cardiovascular and cerebrovascular events) was a composite of all-cause death, myocardial infarction, any revascularization, and stroke. A total of 840 patients were included (206 in the FFR-guided group and 634 in the angiography-guided group). Median follow-up was 7 years (interquartile range, 3.22-11.08 years). After 1:1 propensity-score matching, baseline characteristics between the 2 groups were similar. All-cause death was significantly lower in the FFR-guided group compared with the angiography-guided group (94 [45.6%] versus 119 [57.8%]; hazard ratio [HR], 0.65 [95% CI, 0.49-0.85]; P<0.01). The rate of major adverse cardiovascular and cerebrovascular events was lower in the FFR-guided group (123 [59.7%] versus 139 [67.5%]; HR, 0.75 [95% CI, 0.59-0.95]; P=0.02). Conclusions In patients with reduced left ventricular ejection fraction, deferring revascularization of intermediate coronary stenoses based on FFR is associated with a lower incidence of death and major adverse cardiovascular and cerebrovascular events at 10 years
Infarct size, inflammatory burden, and admission hyperglycemia in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: a multicenter international registry
Background: The inflammatory response occurring in acute myocardial infarction (AMI) has been proposed as a potential pharmacological target. Sodium-glucose co-transporter 2 inhibitors (SGLT2-I) currently receive intense clinical interest in patients with and without diabetes mellitus (DM) for their pleiotropic beneficial effects. We tested the hypothesis that SGLT2-I have anti-inflammatory effects along with glucose-lowering properties. Therefore, we investigated the link between stress hyperglycemia, inflammatory burden, and infarct size in a cohort of type 2 diabetic patients presenting with AMI treated with SGLT2-I versus other oral anti-diabetic (OAD) agents. Methods: In this multicenter international observational registry, consecutive diabetic AMI patients undergoing percutaneous coronary intervention (PCI) between 2018 and 2021 were enrolled. Based on the presence of anti-diabetic therapy at the admission, patients were divided into those receiving SGLT2-I (SGLT-I users) versus other OAD agents (non-SGLT2-I users). The following inflammatory markers were evaluated at different time points: white-blood-cell count, neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), neutrophil-to-platelet ratio (NPR), and C-reactive protein. Infarct size was assessed by echocardiography and by peak troponin levels. Results: The study population consisted of 583 AMI patients (with or without ST-segment elevation): 98 SGLT2-I users and 485 non-SGLT-I users. Hyperglycemia at admission was less prevalent in the SGLT2-I group. Smaller infarct size was observed in patients treated with SGLT2-I compared to non-SGLT2-I group. On admission and at 24 h, inflammatory indices were significantly higher in non-SGLT2-I users compared to SGLT2-I patients, with a significant increase in neutrophil levels at 24 h. At multivariable analysis, the use of SGLT2-I was a significant predictor of reduced inflammatory response (OR 0.457, 95% CI 0.275-0.758, p = 0.002), independently of age, admission creatinine values, and admission glycemia. Conversely, peak troponin values and NSTEMI occurrence were independent predictors of a higher inflammatory status. Conclusions: Type 2 diabetic AMI patients receiving SGLT2-I exhibited significantly reduced inflammatory response and smaller infarct size compared to those receiving other OAD agents, independently of glucose-metabolic control. Our findings are hypothesis generating and provide new insights on the cardioprotective effects of SGLT2-I in the setting of coronary artery disease. Trial registration: Data are part of the ongoing observational registry: SGLT2-I AMI PROTECT. Clinicaltrials: gov Identifier: NCT05261867
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