Delisting of infants and children from the heart transplantation waiting list after carvedilol treatment

AbstractObjectivesWe performed a prospective, randomized, double-blind, placebo-controlled study of carvedilol effects in children with severe, chronic heart failure (HF), despite the use of conventional therapy.BackgroundLittle is known about the effects of carvedilol in youngsters with chronic HF and severe left ventricular (LV) dysfunction.MethodsWe conducted a double-blind, placebo-controlled study of 22 consecutive children with severe LV dysfunction. The children had chronic HF and left ventricular ejection fraction (LVEF) <30%. Patients were randomly assigned to receive either placebo (8 patients) or the beta-blocker carvedilol (14 patients) at 0.01 mg/kg/day titrated up to 0.2 mg/kg/day, followed-up for six months.ResultsDuring the follow-up and the up-titration period in the carvedilol group, four patients died and one underwent heart transplantation. In patients receiving carvedilol evaluated after six months, a significant increase occurred in LVEF, from 17.8% (95% confidence interval [CI], 14.1 to 21.4%) to 34.6% (95% CI, 25.2 to 44.0%); p = 0.001. Modified New York Heart Association (NYHA) functional class improved in nine patients taken off the transplant waiting list. All nine patients were alive at follow-up. In the placebo group, during the six-month follow-up, two patients died, and two underwent heart transplantation. Four patients persisted with HF symptoms (NYHA functional class IV). No significant change occurred in LVEF or fractional shortening.ConclusionsCarvedilol added to standard therapy may reduce HF progression and improve cardiac function, allowing some youngsters to be removed from the heart transplantation waiting list

Local anesthesia with epinephrine is safe and effective for oral surgery in patients with type 2 diabetes mellitus and coronary disease: a prospective randomized study

OBJECTIVE: To investigate the variations in blood glucose levels, hemodynamic effects and patient anxiety scores during tooth extraction in patients with type 2 diabetes mellitus T2DM and coronary disease under local anesthesia with 2% lidocaine with or without epinephrine. STUDY DESIGN: This is a prospective randomized study of 70 patients with T2DM with coronary disease who underwent oral surgery. The study was double blind with respect to the glycemia measurements. Blood glucose levels were continuously monitored for 24 hours using the MiniMed Continuous Glucose Monitoring System. Patients were randomized into two groups: 35 patients received 5.4 mL of 2% lidocaine, and 35 patients received 5.4 mL of 2% lidocaine with 1:100,000 epinephrine. Hemodynamic parameters (blood pressure and heart rate) and anxiety levels were also evaluated. RESULTS: There was no difference in blood glucose levels between the groups at each time point evaluated. Surprisingly, both groups demonstrated a significant decrease in blood glucose levels over time. The groups showed no significant differences in hemodynamic and anxiety status parameters. CONCLUSION: The administration of 5.4 mL of 2% lidocaine with epinephrine neither caused hyperglycemia nor had any significant impact on hemodynamic or anxiety parameters. However, lower blood glucose levels were observed. This is the first report using continuous blood glucose monitoring to show the benefits and lack of side effects of local anesthesia with epinephrine in patients with type 2 diabetes mellitus and coronary disease

In-hospital death in acute coronary syndrome was related to admission glucose in men but not in women

<p>Abstract</p> <p>Background</p> <p>Admission hyperglycaemia is associated with mortality in patients with acute coronary syndrome (ACS), but controversy exists whether hyperglycaemia uniformly affects both genders. We evaluated coronary risk factors, gender, hyperglycaemia and their effect on hospital mortality.</p> <p>Methods</p> <p>959 ACS patients (363 women and 596 men) were grouped based on glycaemia ≥ or < 200 mg/dL and gender: men with glucose < 200 mg/dL (menG-); women with glucose < 200 mg/dL (womenG-); men with glucose ≥ 200 mg/dL (menG+); and women with glucose ≥ 200 mg/dL (womenG+). A logistic regression analysis compared the relation between gender and glycaemia groups and death, adjusted for coronary risk factors and laboratory data.</p> <p>Results group</p> <p>menG- had lower mortality than menG + (OR = 0.172, IC95% 0.062-0.478), and womenG + (OR = 0.275, IC95% 0.090-0.841); womenG- mortality was lower than menG + (OR = 0.230, IC95% 0.074-0.717). No difference was found between menG + vs womenG + (p = 0.461), or womenG- vs womenG + (p = 0.110). Age (OR = 1.067, IC95% 1.031–1.104), EF (OR = 0.942, IC95% 0.915-0.968), and serum creatinine (OR = 1.329, IC95% 1.128-1.566) were other independent factors related to in-hospital death.</p> <p>Conclusions</p> <p>Death was greater in hyperglycemic men compared to lower blood glucose men and women groups, but there was no differences between women groups in respect to glycaemia after adjustment for coronary risk factors.</p

BNP and Admission Glucose as In-Hospital Mortality Predictors in Non-ST Elevation Myocardial Infarction

Objectives. Admission hyperglycemia and B-type natriuretic peptide (BNP) are associated with mortality in acute coronary syndromes, but no study compares their prediction in-hospital death. Methods. Patients with non-ST-elevation myocardial infarction (NSTEMI), in-hospital mortality and two-year mortality or readmission were compared for area under the curve (AUC), sensitivity (SEN), specificity (SPE), positive predictive value (PPV), negative predictive value (NPV), and accuracy (ACC) of glycemia and BNP. Results. Respectively, AUC, SEN, SPE, PPV, NPV, and ACC for prediction of in-hospital mortality were 0.815, 71.4%, 84.3%, 26.3%, 97.4%, and 83.3% for glycemia = 200 mg/dL and 0.748, 71.4%, 68.5%, 15.2%, 96.8% and 68.7% for BNP = 300 pg/mL. AUC of glycemia was similar to BNP (P = 0.411). In multivariate analysis we found glycemia ≥200mg/dL related to in-hospital death (P = 0.004). No difference was found in two-year mortality or readmission in BNP or hyperglycemic subgroups. Conclusion. Hyperglycemia was an independent risk factor for in-hospital mortality in NSTEMI and had a good ROC curve level. Hyperglycemia and BNP, although poor in-hospital predictors of unfavorable events, were independent risk factors for death or length of stay >10 days. No relation was found between hyperglycemia or BNP and long-term events

Mycoplasma pneumoniae and Chlamydia pneumoniae in calcified nodules of aortic stenotic valves

Estenose da Valva Aórtica (EVA) tem sido considerada como um processo aterosclerótico das valvas pois elas freqüentemente exibem alterações inflamatórias com acúmulo de macrófagos e linfócitos T, bem como infiltração de lípides. O presente estudo investigou se as bactérias Chlamydia pneumoniae (CP) e Mycoplasma pneumoniae (MP), detectadas previamente em placas ateroscleróticas, estavam presentes na EVA. Dez valvas removidas cirúrgicamente de pacientes com EVA foram analisadas pela imunohistoquímica, hibridização in situ e microscopia eletrônica. A média e desvio padrão das porcentagens de área ocupadas por antígenos de CP e de DNA do MP foram respectivamente de 6,21 +/- 5,41 e 2,27 +/- 2,06 nos focos de calcificação; 2,8 +/- 3,33 e 1,78+/- 3,063 nas áreas de fibrose ao redor e 0,21 +/- 0,17 e 0,12 +/- 0,13 nas regiões menos lesadas da válvula. Houve uma maior quantidade de CP e MP nos focos de calcificação e na fibrose ao redor do que nas regiões valvulares mais preservadas. Em conclusão, o fato de haver maior quantidade de CP e MP nos focos de calcificação da EVA favorece a hipótese de que a estenose aórtica não é um processo degenerativo inevitável devido a idade, mas sim uma resposta inflamatória à presença dessas bactérias, em uma morfologia semelhante à detectada na injúria aterosclerótica.Aortic Valve Stenosis (AVS) has been explained as an atherosclerotic process of the valve as they often exhibit inflammatory changes with infiltration of macrophages, T lymphocytes and lipid infiltration. The present study investigated whether the bacteria Chlamydia pneumoniae (CP) and Mycoplasma pneumoniae (MP), detected previously in atherosclerotic plaques, are also present in AVS. Ten valves surgically removed from patients with AVS were analyzed by immunohistochemistry, in situ hybridization, and electron microscopy. The mean and standard deviation of the percentage areas occupied by CP antigens and MP - DNA were respectively 6.21 +/- 5.41 and 2.27 +/- 2.06 in calcified foci; 2.8 +/- 3.33 and 1.78+/- 3.63 in surrounding fibrotic areas, and 0.21 +/- 0.17 and 0.12 +/- 0.13 in less injured parts of the valve. There was higher amount of CP and MP in the calcified foci and in the surrounded fibrosis than in more preserved valvular regions. In conclusion, the fact that there were greater amounts of CP and MP in calcification foci of AVS favors the hypothesis that AS is not an inevitable degenerative process due to aging, but rather that it may be a response to the presence of these bacteria, similarly to the morphology detected in atherosclerosis damage

Atheromas that cause fatal thrombosis are usually large and frequently accompanied by vessel enlargement

Several lines of clinical evidence show that AMI frequently occurs at sites with mild to moderate degree of coronary stenosis. The degree of luminal stenosis depends on plaque deposition and degree of vessel remodeling, features poorly assessed by coronary angiography. This postmortem study tested the hypothesis that the size of coronary atheroma and the type of remodeling distinguish culprit lesion responsible for fatal AMI from equi-stenotic nonculprit lesion in the same coronary tree. The main coronary branches from 36 consecutive patients with fatal AMI were studied. The culprit lesion (Group 1) and an equi-stenotic nonculprit segment (Group 2) obtained in measurements of another coronary branch from the same patient were compared. Morphometry and plaque composition was assessed in both groups. Compared to Group 2, Group 1 had larger areas of: plaque $9.6 vs. 4.7 mm^2$, vessel $12.7 vs. 7.4 mm^2$ and lumen $1.7 vs. 1.2 mm^2$; (P<.01). Positive remodeling was more frequent in Group 1 than Group 2: 21/30 (70%) vs. 8/26 (31%). Plaque area correlated positively with lipid core and macrophages and negatively with fibrosis and smooth muscle cells. Atherosclerotic plaques that cause fatal thrombosis are more frequently positively remodeled and tend to be larger than nonculprit plaques with the same degree of cross-sectional stenosis. We tested whether arterial remodeling and plaque size vary between segments containing a fatal thrombosed plaque versus an equi-stenotic nonculprit plaque. Culprit vessel segments had higher cross-sectional areas of intimal plaque and of vessel wall than equi-stenotic nonculprit plaques. The cross-sectional area of the vessel correlated positively with both the lipid core area and $CD68^+$ macrophage content, and negatively with fibrosis area and smooth muscle cell content. These results add elements explaining limitations of angiography in identifying plaques and provide new insights into the role of remodeling in plaque instability.Other Research Uni