Stuart G. Lehrman

Prevalence of Moderate or Severe Left Ventricular Diastolic Dysfunction in Obese Persons with Obstructive Sleep Apnea

We investigated prior to gastric bypass surgery the prevalence of left ventricular diastolic dysfunction (LVDD) by Doppler and tissue Doppler echocardiography in 14 obese women and in 6 obese men, mean age 45 years, with a mean body mass index of 49 ± 5 kg/m2 who had nocturnal polysomnography for obstructive sleep apnea (OSA). The Doppler and tissue Doppler echocardiographic data were analyzed blindly without knowledge of the clinical characteristics or whether OSA was present or absent. Of 20 patients, 8 (40%) had no OSA, 4 (20%) had mild OSA, and 8 (40%) had moderate or severe OSA. Moderate or severe LVDD was present in 4 of 8 patients (50%) with moderate or severe OSA and in none of 12 patients (0%) with no or mild OSA (p < 0.01). Obese patients with moderate or severe OSA have a higher prevalence of moderate or severe LVDD than obese patients with no or mild OSA.

Prevalence of left ventricular hypertrophy in persons with and without obstructive sleep apnea.

We investigated the prevalence of left ventricular hypertrophy (LVH) in persons with and without obstructive sleep apnea (OSA). Fifty-three persons had a nocturnal polysomnogram to diagnose OSA and 2-dimensional echocardiograms to measure left ventricular mass. OSA was considered mild if the respiratory disturbance index (RDI) was 5 to 15, moderate if the RDI was 15 to 30, and severe if the RDI was >30. LVH was diagnosed if the left ventricular mass index was >110 g/m2 in women and >134 g/m2 in men. LVH was present in 21 of 27 persons (78%) with moderate or severe OSA, in 6 of 13 persons (46%) with mild OSA, and in 3 of 13 persons (23%) with no OSA (P < 0.001 comparing moderate or severe OSA with no OSA and P < 0.05 comparing moderate or severe OSA with mild OSA). OSA was a significant independent predictor of LVH after controlling the confounding effects of hypertension with an odds ratio of 3.579 (95% confidence interval, 1.589–8.058).

Management of massive and nonmassive pulmonary embolism

Massive pulmonary embolism (PE) is characterized by systemic hypotension (defined as a systolic arterial pressure < 90 mm Hg or a drop in systolic arterial pressure of at least 40 mm Hg for at least 15 min which is not caused by new onset arrhythmias) or shock (manifested by evidence of tissue hypoperfusion and hypoxia, including an altered level of consciousness, oliguria, or cool, clammy extremities). Massive pulmonary embolism has a high mortality rate despite advances in diagnosis and therapy. A subgroup of patients with nonmassive PE who are hemodynamically stable but with right ventricular (RV) dysfunction or hypokinesis confirmed by echocardiography is classified as submassive PE. Their prognosis is different from that of others with non-massive PE and normal RV function. This article attempts to review the evidence-based risk stratification, diagnosis, initial stabilization, and management of massive and nonmassive pulmonary embolism.

Cardiovascular consequences of sleep-related breathing disorders.

Sleep-related breathing disorders (SRBDs) represent a spectrum of abnormalities that range from simple snoring to upper airway resistance syndrome to sleep apnea. The clinical presentation may include obesity, snoring, neuropsychological dysfunction, and daytime hypersomnolence and tiredness. The acute hemodynamic alterations of obstructive sleep apnea include systemic and pulmonary hypertension, increased right and left ventricular afterload, and increased cardiac output. Earlier reports attributed the coexistence of SRBDs with cardiovascular diseases to the shared risk factors such as age, sex, and obesity. However, recent epidemiologic data confirm an independent association between SRBDs and the different manifestations of cardiovascular diseases. Possible mechanisms may include a combination of intermittent hypoxia and hypercapnia, repeated arousals, sustained increase in sympathetic tone, reduced baroreflex sensitivity, increased platelet aggregation, and elevated plasma fibrinogen and homocysteine levels. The strength of the association, its pathogenesis, and the impact of treatment of SRBDs on the health outcome of patients with cardiovascular diseases are issues to be addressed in future studies.

Management of massive and submassive pulmonary embolism.

Massive pulmonary embolism has a high mortality rate despite advances in diagnosis and therapy. This article attempts to review the evidence-based risk stratification, diagnosis, initial stabilization, and management of massive and submassive pulmonary embolism.

Amiodarone induced pulmonary toxicity: An unusual response to steroids

Summary Background: Amiodarone, class III anti-arrhythmic was originally introduced to treat angina pectoris, was later approved by FDA in 1985 for the treatment of ventricular arrhythmias. Despite its anti-arrhythmic properties, amiodarone is associated with side effects such as thyroid dysfunction, corneal deposits, bluish skin discoloration, neuropathy and pulmonary toxicity. Amiodarone induced pulmonary toxicity (AIPT) is one of the most serious side effect thus limiting its use. Case Report: We encountered a 66 year old male with early onset AIPT who presented with dyspnea and chest imaging revealed extensive ground-glass opacities throughout lung parenchyma with rapid resolution of these opacities in a week following treatment with corticosteroids. Conclusions: There have been few case reports of AIPT with complete resolution of ground glass opacities on treatment with corticosteroids, but none demonstrated a rapid response to corticosteroids. Heath care providers should withdraw amiodarone at the earliest suspicion (as illustrated in our case); any delay can potentially be fatal. This case highlights the fact that AIPT is a reversible phenomenon, provided its early recognition and treatment before fibrosis sets in This case also highlights the need to include AIPT in the differential diagnosis in any patient on amiodarone who presents with shortness of breath.

Association of Lung Volumes With Nocturnal Oxygen Saturation in Obese Persons: A Possible Role for Therapeutic Continuous Positive Airway Pressure

We investigated the association among obesity, nocturnal oxygen saturation, and pulmonary function in 31 obese women and 17 obese men scheduled for bariatric surgery who underwent nocturnal polysomnography and pulmonary function testing. Pearson correlation coefficients showed a significant association between expiratory reserve volume percent and average oxygen saturation (P = 0.027), between body mass index and lowest oxygen saturation (P = 0.034), and between body mass index and average oxygen saturation (P = 0.039). The mean age, body mass index, expiratory reserve volume percent, and functional residual capacity percent were not significantly different between obese women and men. The lowest oxygen saturation was 80 ± 10% in obese women and 62 ± 19% in obese men (P = 0.001). The average oxygen saturation was 88 ± 5% in obese women and 83 ± 6% in obese men (P = 0.005) Therapeutic nocturnal continuous positive airway pressure may have a role by improving ventilation-perfusion matching and thereby improving nocturnal oxygen saturation in these patients.

Can echocardiographically estimated pulmonary arterial elastance be a non-invasive predictor of pulmonary vascular resistance?

Introduction Measurement of pulmonary vascular resistance (PVR) is essential in evaluating a patient with pulmonary hypertension. Material and methods Data from right heart catheterization (RHC) and echocardiograms performed within 90 days of each other on 45 non-consecutive adult patients were reviewed in this retrospective study. Patients were recruited using an assortment of strategies to ensure the presence of patients with a wide range of PVR. Results The linear regression equation between RHC-derived PVR and echocardiographic pulmonary arterial elastance (PAE) was: PVR = (562.6 × PAE) – 38.9 (R = 0.56, p < 0.0001). An adjustment for echocardiographic PAE was made by multiplying it by hemoglobin (in g/dl) and (right atrial area)1.5 (in cm3). As RHC-derived PVR varies with blood hemoglobin, an adjustment for PVR was made for hemoglobin of 12 g/dl. Visualization of the XY scatter plot of adjusted PVR and adjusted PAE isolated a subset of patients with PVR higher than 8.8 Wood units, where a strong linear relationship existed (adjusted PVR = (0.89 × adjusted PAE) + 137.4, R = 0.89, p = 0.008). Conclusions The correlation coefficient of the regression equation connecting echocardiographic PAE and RHC-derived PVR was moderate. In a subset of patients with very high PVR and after appropriate adjustment, a strong linear relationship existed with an excellent correlation coefficient.

Prevalence of use of cardiovascular drugs in 499 patients with suspected coronary artery disease at time of hospitalization for coronary angiography and in 357 patients with obstructive coronary artery disease documented by coronary angiography.

In a prospective study of 499 patients with suspected coronary artery disease (CAD) hospitalized for coronary angiography, the prevalence of use of cardiovascular drugs at hospital admission was 80% for antiplatelet drugs, 66% for beta blockers, 55% for angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), 65% for lipid-lowering drugs, 24% for calcium channel blockers (CCBs), and 16% for nitrates. In 357 patients with obstructive CAD diagnosed by coronary angiography, the prevalence of use of these drugs at hospital discharge was 100% for antiplatelet drugs, 97% for beta blockers, 91% for ACE inhibitors or ARBs, 98% for lipid-lowering drugs, 17% for CCBs, and 27% for nitrates. Obstructive CAD was significantly more prevalent in men (P < 0.025), in cigarette smokers (P < 0.01), and in patients with hypertension, diabetes, or hypercholesterolemia (P < 0.001). Age, race, body mass index, and neck circumference were not significantly different for patients with versus without obstructive CAD.

Lack of Significant Bronchial Reactivity to Inhaled Normal Saline in Subjects with a Positive Methacholine Challenge Test

Patients with symptoms suggestive of asthma often have normal resting pulmonary function. In these patients, a determination of airway responsiveness by bronchial challenge is useful in demonstrating bronchial hyperreactivity (BHR), a defining feature of asthma. In the methacholine (Mch) challenge, it is recommended that following a baseline measurement of FEV1, the patient inhale the normal saline (NS) diluent and FEV1 be repeated to assess for nonspecific BHR to NS. It is also recommended that post-NS inhalation FEV1 should be used as the control value from which decrement in FEV1 is compared following Mch challenge. Mch testing was performed in 44 patients with symptoms suggestive of asthma (cough, chest tightness, dyspnea) and normal resting pulmonary function. Baseline spirometry was obtained and repeated after inhalation of NS and after five breaths each of Mch at the following concentrations: 0.025 mg/ml, 0.25 mg/ml, 2.5 mg/ml, 10 mg/ml, and 25 mg/ml. The procedure was terminated when FEV1 decreased to at least 80% of the post-NS value or if the maximal concentration of Mch had been reached. The post-NS FEV1 value was > or = 91% of the pre-NS value in all the subjects range 91-105%). Using the post-NS FEV1 as the recommended control value, 20 patients (45%) had a positive Mch challenge and 24 patients (55%) had a negative Mch challenge. Had we used the pre-NS FEV1 as a control value, only 2 patients would have been reclassified, and when these 2 cases are carefully examined, there would have been no significant change in the clinical interpretation of the MCh test.(ABSTRACT TRUNCATED AT 250 WORDS)