Cardiopulmonary Testing before Pediatric Adenotonsillectomy for Severe and Very Severe Obstructive Sleep Apnea Syndrome.

OBJECTIVES/HYPOTHESIS: Adenotonsillectomy is first-line treatment for pediatric obstructive sleep apnea syndrome (OSAS) when not otherwise contraindicated. There is concern severe OSAS increases risk of comorbid cardiopulmonary abnormalities, such as ventricular hypertrophy or pulmonary hypertension, which preoperative testing could detect. Our objective is to determine if there is a severity of pediatric OSAS where previously undetected cardiopulmonary comorbidities are likely. STUDY DESIGN: Retrospective chart review. METHODS: We performed a retrospective review of 358 patients ≤21 years with severe OSAS who underwent adenotonsillectomy at a tertiary hospital June 1, 2016 to June 1, 2018. We extracted demographics, comorbidities, polysomnography, and preoperative tests. Wilcoxon rank-sum and logistic regression estimated associations of OSAS severity (based on obstructive apnea-hypopnea index [OAHI], hypoxia, hypercarbia) with preoperative echocardiograms and chest X-rays (CXRs). RESULTS: Mean age was 5.9 (±3.6) years and 52% were male. Mean OAHI and oxygen saturation nadir were 30.3 (±23.8) and 80.7% (±9.2), respectively. OAHI ≥60 was associated with having a preoperative echocardiogram (OR, 3.8; 95% CI, 1.7-8.5) or CXR (OR, 3.0; 95% CI, 1.4-6.8) compared to OAHI 10-59. There were no significant associations between OSAS severity and test abnormalities. The presence of previously diagnosed cardiopulmonary comorbidities was associated with abnormalities on echocardiogram (OR, 36; 95% CI, 4.1-320.1) and CXR (OR, 4.1; 95% CI, 1.2-14.4). CONCLUSIONS: Although pediatric patients with very severe OSAS (OAHI ≥60) underwent more pre-adenotonsillectomy cardiopulmonary tests, OSAS severity did not predict abnormal findings. Known cardiopulmonary comorbidities may be a better indication for cardiopulmonary testing than polysomnographic parameters, which could streamline pre-adenotonsillectomy evaluation and reduce cost. LEVEL OF EVIDENCE: 4 Laryngoscope, 131:2361-2368, 2021.

Effect of the 2010 task force criteria on reclassification of cardiovascular magnetic resonance criteria for arrhythmogenic right ventricular cardiomyopathy.

BACKGROUND: We sought to evaluate the effect of application of the revised 2010 Task Force Criteria (TFC) on the prevalence of major and minor Cardiovascular Magnetic Resonance (CMR) criteria for Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) versus application of the original 1994 TFC. We also assessed the utility of MRI to identify alternative diagnoses for patients referred for ARVC evaluation. METHODS: 968 consecutive patients referred to our institution for CMR with clinical suspicion of ARVC from 1995 to 2010, were evaluated for the presence of major and minor CMR criteria per the 1994 and 2010 ARVC TFC. CMR criteria included right ventricle (RV) dilatation, reduced RV ejection fraction, RV aneurysm, or regional RV wall motion abnormalities. When quantitative measures of RV size and function were not available, and in whom abnormal size or function was reported, a repeat quantitative analysis by 2 qualified CMR physicians in consensus. RESULTS: Of 968 patients, 220 (22.7%) fulfilled either a major or a minor 1994 TFC, and 25 (2.6%) fulfilled any of the 2010 TFC criterion. Among patients meeting any 1994 criteria, only 25 (11.4%) met at least one 2010 criterion. All patients who fulfilled a 2010 criteria also satisfied at least one 1994 criterion. Per the 2010 TFC, 21 (2.2%) patients met major criteria and 4 (0.4%) patients fulfilled at least one minor criterion. Eight patients meeting 1994 minor criteria were reclassified as satisfying 2010 major criteria, while 4 patients fulfilling 1994 major criteria were reclassified to only minor or no criteria under the 2010 TFC.Eighty-nine (9.2%) patients had alternative cardiac diagnoses, including 43 (4.4%) with clinically significant potential ARVC mimics. These included cardiac sarcoidosis, RV volume overload conditions, and other cardiomyopathies. CONCLUSIONS: Application of the 2010 TFC resulted in reduction of total patients meeting any diagnostic CMR criteria for ARVC from 22.7% to 2.6% versus the 1994 TFC. CMR identified alternative cardiac diagnoses in 9.2% of patients, and 4.4% of the diagnoses were potential mimics of ARVC.

Right ventricular enlargement on chest computed tomography: a predictor of early death in acute pulmonary embolism.

BACKGROUND: In patients with acute pulmonary embolism (PE), rapid and accurate risk assessment is paramount in selecting the appropriate treatment strategy. Right ventricular (RV) enlargement on chest CT has previously been shown to correlate with an unstable hospital course, but its role as a predictor of death is unknown. METHODS AND RESULTS: We evaluated 431 consecutive patients (mean age, 59+/-16 years; 55% women) with acute PE confirmed by multidetector-row chest CT. With the use of multiplanar reformats of axial CT data, CT 4-chamber (4-CH) views were reconstructed and right and left ventricular dimensions (RV(D), LV(D)) were measured. RV enlargement, defined as RV(D)/LV(D) >0.9, was present in 276 (64.0%; 95% CI, 59.5% to 68.6%) patients. Thirty-day mortality rate was 15.6% (95% CI, 11.3% to 19.9%) in patients with and 7.7% (95% CI, 3.5% to 12.0%) without RV enlargement (log rank, P=0.018). The hazard ratio of RV(D)/LV(D) >0.9 for predicting 30-day death was 3.36 (95% CI, 1.13 to 9.97; P=0.029). On multivariable analysis, RV enlargement predicted 30-day death (hazard ratio, 5.17; 95% CI, 1.63 to 16.35; P=0.005) after adjusting for pneumonia (hazard ratio, 2.95; 95% CI, 1.19 to 3.83; P=0.002), cancer (hazard ratio, 2.13; 95% CI, 1.19 to 3.83; P=0.011), chronic lung disease (hazard ratio, 2.00; 95% CI, 1.04 to 3.86; P=0.039), and age (hazard ratio, 1.03; 95% CI, 1.01 to 1.05; P=0.005). CONCLUSIONS: In patients with acute PE, RV enlargement on reconstructed CT 4-CH view helps predict early death.

[Myocardial inotropic function in patients with chronic obstructive lung diseases as evidenced by biventricular equilibrium ventriculography]. / Sostoianie inotropnoi funktsii miokarda u bol'nykh khronicheskimi obstruktivnymi bolezniami legkikh po dannym biventrikuliarnoi ravnovesnoi vebtrikulografii.

At present chronic obstructive lung diseases (COLD) occupy a prominent place in the morbidity and mortality of the adult population, with regarding the more and more increasing influence of aggressive environmental factors (sulfur dioxide, nitrogen, ozone, black smog and smoking). Due to the fact that clinical symptoms develop in patients with COLD at its late stages when there are irreversible changes in not only the bronchopulmonary apparatus, but, to a greater extent, the cardiovascular system; the efficiency of performed therapy is rather little. This shows it necessary to diagnose myocardial contractile disorders in such patients as soon as possible as the routine accessible cardiac study techniques (ECG, EchoCG) are of low informative value due to significant emphysema. In this view, of particular value is the use of radionuclide studies, including biventricular equilibrium radionuclide ventriculography that provides adequate information on the status of both ventricles.

Clinical predictors of pulmonary hypertension in patients undergoing liver transplant evaluation.

Clinical prediction of portopulmonary hypertension (PPHTN) is critical in the preoperative evaluation of candidates for orthotopic liver transplantation (OLT) because of its association with significant morbidity and mortality. To determine the clinical, laboratory, and echocardiographic predictors of PPHTN, we retrospectively evaluated 55 candidates before OLT. From those, 8 candidates had pulmonary hypertension ([HTN] group A) and 47 candidates did not (group B). Pulmonary HTN was defined as a mean pulmonary artery pressure (PAP) of 25 mm Hg or greater and either elevated pulmonary vascular resistance or normal pulmonary artery wedge pressure. The significant predictors of PPHTN were (1) systemic arterial HTN (63% in group A v 9% in group B; P <.001), (2) loud pulmonary component of the second heart sound (38% v 2%; P =. 001), (3) right ventricular (RV) heave (38% v 4%; P =.002), (4) RV dilatation by echocardiogram (63% v 0%; P <.001), (5) RV hypertrophy by echocardiogram (38% v 0%; P =.001), and (6) echocardiogram-estimated systolic PAP (SPAP) greater than 40 mm Hg (63% v 2%; P <.001). The sensitivity of these variables for the detection of pulmonary HTN ranges from 37% to 63%, and their specificity from 91% to 100%. We conclude that several clinical and echocardiographic features are significantly associated with pulmonary HTN in patients with cirrhosis. In particular, echocardiogram-estimated SPAP greater than 40 mm Hg is strongly associated with pulmonary HTN and is specific. These predictors, however, are not sensitive enough to identify all the patients with PPHTN. Therefore, the evaluation of a combination of these variables may be useful for the preoperative identification of pulmonary HTN in liver transplant candidates.

Specificity of electrocardiographic myocardial infarction screening criteria in patients with nonischemic cardiomyopathies.

BACKGROUND: The 32-point, 54-criteria Selvester QRS scoring system has been successfully used to estimate the size of nonacute myocardial infarction (MI). Three criteria of the system have been shown to be sensitive for the identification of nonacute MI and specific in normal control subjects. The validity of the system has not been tested in patients with cardiomyopathy of nonischemic origin. The purpose of this study was to examine the electrocardiographs (ECGs) of patients with abnormal left ventricular function but no presence of coronary disease to determine the diagnostic specificity of the MI screening criteria subset of the Selvester QRS scoring system. METHODS AND RESULTS: Six hundred ninety patients were considered. Exclusion criteria included age <10 years, cardiac transplantation, thrombolytic therapy, any angiographic evidence of coronary disease, left ventricular ejection fraction (LVEF) >60%, or history of myocardial revascularization. ECG exclusion criteria included left ventricular hypertrophy, right ventricular hypertrophy, left bundle branch block, right bundle branch block, ventricular pacing, left anterior fascicular block, left posterior fascicular block, ventricular preexcitation, and low voltage, because these confounding factors could mimic an infarct on the ECG. The 261 remaining patients were then examined for the presence of the MI screening criteria subset: (1) inferior location: Q > or =30 msec in aVF, (2) anterior location: either any Q or R< or =0.1 mV and < or =10 msec in V2, and (3) posterior location: R> or =40 msec in V1. Thirty-two of the 261 patients falsely met at least 1 of the 3 MI screening criteria, resulting in an overall specificity of 88% (vs 95% in normal control subjects, P=.0006). A specificity of 98% (n = 256) was achieved for the inferior MI screening criterion alone, whereas the anterior and posterior MI screening criteria alone achieved significantly lower specificities: 94% (n = 245) and 95% (n = 249), respectively. When the patient population was divided into LVEF <30% and LVEF > or =30%, no significant association was found between MI screening criteria and LVEF with specificities of 87% and 88%, respectively, for the 2 groups (P= .34). CONCLUSIONS: The MI screening criteria subset is relatively specific in patients with nonischemic cardiomyopathy, falsely identifying only 12% with nonacute MI. However, this specificity is lower than the 95% achieved in normal subjects. Regional accumulation of scarring caused by cardiomyopathy could result in false-positive indication of MI in the present population. Another possibility could be that some patients could have hypertrophy of the myocardium insufficient to produce positive ECG criteria for left ventricular hypertrophy or right ventricular hypertrophy but sufficient to mimic infarction.

Effect of dietary flax oil and hypobaric hypoxia on right ventricular hypertrophy and ascites in broiler chickens.

1. The effect of dietary flax oil on growth rate, blood haemoglobin content, mortality and incidence of pulmonary hypertension and ascites in broilers at ambient pressure and at reduced atmospheric pressure was examined. 2. Birds were housed either in hypobaric chambers simulating 1000, 1500 or 2200 m altitude or in pens at ambient atmospheric pressure and fed on diets containing 100 g/kg added fat as either an animal/vegetable (A/V) blend or flax oil. 3. Birds raised under hypobaric conditions had a decreased growth rate and increased mortality, blood haemoglobin content, and incidence of pulmonary hypertension and ascites compared to the groups at normal atmospheric pressure. 4. Broilers fed on the diet containing flax oil showed no difference in growth rate or blood haemoglobin content compared to birds fed on the A/V fat diet raised at the same altitude. 5. Inclusion of flax oil in the diet decreased mortality and the incidence of ascites at 2200 m and pulmonary hypertension at 1500 m. 6. Flax oil may be an effective method of reducing ascites and pulmonary hypertension in broilers without affecting performance.

Relation between cardiovascular pathologic conditions and malignant tumours as seen by pathologist. I. Frequency of malignant neoplasms in the population with myocardial hypertrophy as seen by pathologist.

Relatively low co-existence of malignant neoplasms and chronic cardiovascular disease was documented in this work the emphasis being put on the conditions running with myocardial hypertrophy. The percentage of malignancy in the total autopsy material of 5821 men and 6849 women was 27.8 and 23.0 resp., and in the subgroup with heart weight 300-400 g, 36.8 and 31.0 resp. This percentage was significantly lower in separated subgroups of: a. arterial hypertension, 6.6 and 10.2, b. cardio-pulmonary syndrome, 23.0 and 18.5, c. healed myocardial infarct accompanied by myocardial hypertrophy, 13.3 and 11.7, d. acquired valvar deformity, 15.3 and 10.1. The subgroup of heart weight 150-250 g showed 57.2% and 46.6% of cases with malignancy while that of cardiac weight over 600 g-7.4% and 5.7%. In the subgroup of normal right-(2-3 mm) and left-ventricular (10-12 mm) wall thickness corresponding percentage equalled 29.4 and 30.1, in the subgroup of right-ventricular wall thickness over 6 mm--14.4 and 8.8, and in that of left-ventricular wall thickness over 18 mm--12.5 and 9.4. Scanty available information suggests some antimitotic activity of catecholamines believed to condition that of chalones. Catecholamines are also attributed with the stimulation of myocardial hypertrophy. The correlation of our findings with assumptions mentioned above seem to justify a hypothesis, or only a possibility, that compensatory mechanisms active in the cardiovascular diseases create an unfavourable background for the development of neoplasm.

Propranolol reduces myocardial hypertrophy in the right cardiac chambers after infarction in rats.

The effects of chronic propranolol (Prop) therapy on the postinfarction myocardial hypertrophy of infarcted rats were studied by histological techniques. Male albino rats were submitted to left coronary artery ligation to produce infarction or to sham surgery (Con, N = 6). Infarcted rats (Inf) were divided into 2 groups receiving Prop (2.5 mg/kg, twice a day, N = 6) or saline (N = 6) for one month, respectively. Myocyte diameters were measured in longitudinally oriented sections in the four heart chambers (60 cells/chamber). Inf produced a significant increase in mean diameter of myocytes from the right atrium and ventricle and from the left atrium. In the right ventricle, myocyte diameter increased from 8.9 +/- 0.5 microns in the Con group to 12.5 +/- 0.6 microns in the Inf group (P < 0.05). Under Prop, myocyte diameter was reduced (P < 0.05) to 9.8 +/- 0.9 microns. Similar values were observed in the right atrium. In the left atrium, Prop produced only a partial reversion of the postinfarction hypertrophy. In the left ventricle, myocyte diameter was not significantly changed after Inf or Prop therapy. These data show that beta blockers reduce the myocardial hypertrophy in the right heart chambers after experimental infarcts in rats. This effect can be secondary to reduction of pulmonary hypertension or to blockade of direct effects of catecholamines on myocardial fibers or both.