Effect of obstructive sleep apnea on mitral valve tenting.

Obstructive apneas produce high negative intrathoracic pressure which imposes an afterload burden on the left ventricle. Such episodes might produce structural changes in the left ventricle over time. Doppler echocardiograms were obtained within 2 months of attended polysomnography. Patients were grouped according to apnea-hypopnea index (AHI): mild/no OSA (AHI \u3c 15) and mod/severe OSA (AHI ≥ 15). Mitral valve tenting height and area, left ventricular (LV) long and short axis, and LV end-diastolic volume (LVEDV), were measured along with tissue Doppler parameters. Comparisons of measurements at baseline and follow up between and within groups were obtained; correlations between absolute changes (deltas) in echocardiographic parameters were also performed. After a mean follow up of 240 days mitral valve tenting height increased significantly (1.17 ± 0.12 cm to 1.28 ± 0.17 cm, p=0.001) in mod/severe OSA as did tenting area (2.30 ± 0.41 cm2 to 2.66 ± 0.60 cm2, p=0.0002); delta tenting height correlated with delta LVEDV (rho 0.43, p=0.01) and delta tenting area (rho 0.35, p=0.04). In mild/no OSA patients there was no significant change in tenting height; there was a borderline significant increase in tenting area (2.20 ± 0.44 cm2 to 2.31 ± 0.43 cm2, p=0.05). Septal E’ decreased (8.04 ± 2.49 cm/sec to 7.10 ± 1.83 cm/sec, p=0.005) in mod/severe OSA subjects, but not in the mild/no OSA group. In conclusion, in patients with mod/severe OSA, mitral valve tenting height and tenting area increase significantly over time. This appears to be related, at least in part, to changes in LV geometry

Association between QRS duration and obstructive sleep apnea.

BACKGROUND: Both obstructive sleep apnea (OSA) and prolonged QRS duration are associated with hypertension, heart failure, and sudden cardiac death. However, possible links between QRS duration and OSA have not been explored. METHODS: Cross-sectional study of 221 patients who underwent polysomnography at our center. Demographics, cardiovascular risk factors and ECG were collected to explore a relationship between OSA and QRS duration. RESULTS: The apnea-hypopnea index (AHI) was positively correlated with QRS duration (r = 0.141, p = 0.03). Patients were divided into 3 groups: AHI \u3c 5 (61), AHI 5-29 (104), and AHI \u3e 30 (55). The mean QRS duration prolonged significantly as OSA worsened (AHI \u3c 5, 85 ± 9.5; AHI 5-29, 89 ± 11.9; and AHI \u3e 30, 95 ± 19.9 ms, p = 0.001). QRS ≥ 100 ms was present in 12.7% of patients with severe OSA compared with 0% in the rest of the sample (p \u3c 0.0001). After adjustment for age, race, and cardiovascular risk factors, this association remained significant in women but not in men. CONCLUSION: QRS duration and OSA were significantly associated. Severity of OSA independently predicted prolonged QRS in women but not men. Nevertheless, prolongation of QRS duration in either sex may potentiate arrhythmic risks associated with OSA

Association between obesity and infarct size: insight into the obesity paradox.

Abstract: Background: In patients with coronary heart disease, being overweight or obese is associated with better outcomes, a phenomenon known as the \u27obesity paradox\u27. Despite the high prevalence of obesity in the United Sates, its effects on infarct size are largely unexplored. Methods: Prospective cross-sectional study of 102 consecutive patients admitted with acute myocardial infarction (MI). Standardized forms were used to collect data on body mass index (BMI), waist circumference (WC), cardiovascular risk factors, and medications. Peak troponin I and creatinine phosphokinase (CPK) were used to estimate infarct size. Epicardial and pericardial fat were measured by echocardiography. We used univariate and multivariate analyses to assess whether obesity was associated with infarct size. Correlations between BMI, WC and cardiac fat with cardiac biomarkers were also performed. Results: Mean age was 62±12 years, and 55% were men. Obesity was diagnosed in 69%. On multivariate analysis, obesity was associated with greater infarct size in non-ST elevation MI (p=0.02). A positive correlation was observed between BMI and peak troponin I (rho=0.24, p=0.03), and both, BMI and WC had a positive correlations with CPK levels (rho=0.28, & rho=0.28, both p=0.02). However, in ST elevation MI, obesity was associated with smaller infarct size (p=0.05). Epicardial fat + pericardial fat had a negative correlation with peak CPK levels (rho=-0.36, p=0.05). Conclusions: We observed an opposite association between obesity and infarct size depending on the type of MI. These results were unexpected and may provide insight into the pathophysiology of the obesity paradox

Dynamic changes of left ventricular performance and left atrial volume induced by the mueller maneuver in healthy young adults and implications for obstructive sleep apnea, atrial fibrillation, and heart failure.

Using the Mueller maneuver (MM) to simulate obstructive sleep apnea (OSA), our aim was to investigate acute changes in left-sided cardiac morphologic characteristics and function which might develop with apneas occurring during sleep. Strong evidence supports a relation between OSA and both atrial fibrillation and heart failure. However, acute effects of airway obstruction on cardiac structure and function have not been well defined. In addition, it is unclear how OSA might contribute to the development of atrial fibrillation and heart failure. Echocardiography was used in healthy young adults to measure various parameters of cardiac structure and function. Subjects were studied at baseline, during, and immediately after performance of the MM and after a 10-minute recovery. Continuous heart rate, blood pressure, and pulse oximetry measurements were made. During the MM, left atrial (LA) volume index markedly decreased. Left ventricular (LV) end-systolic dimension increased in association with a decrease in LV ejection fraction. On release of the maneuver, there was a compensatory increase in blood flow to the left side of the heart, with stroke volume, ejection fraction, and cardiac output exceeding baseline. After 10 minutes of recovery, all parameters returned to baseline. In conclusion, sudden imposition of severe negative intrathoracic pressure led to an abrupt decrease in LA volume and a decrease in LV systolic performance. These changes reflected an increase in LV afterload. Repeated swings in afterload burden and chamber volumes may have implications for the future development of atrial fibrillation and heart failure

Day-night variation of acute myocardial infarction in obstructive sleep apnea.

OBJECTIVES: This study sought to evaluate the day-night variation of acute myocardial infarction (MI) in patients with obstructive sleep apnea (OSA). BACKGROUND: Obstructive sleep apnea has a high prevalence and is characterized by acute nocturnal hemodynamic and neurohormonal abnormalities that may increase the risk of MI during the night. METHODS: We prospectively studied 92 patients with MI for which the time of onset of chest pain was clearly identified. The presence of OSA was determined by overnight polysomnography. RESULTS: For patients with and without OSA, we compared the frequency of MI during different intervals of the day based on the onset time of chest pain. The groups had similar prevalence of comorbidities. Myocardial infarction occurred between 12 am and 6 am in 32% of OSA patients and 7% of non-OSA patients (p = 0.01). The odds of having OSA in those patients whose MI occurred between 12 am and 6 am was 6-fold higher than in the remaining 18 h of the day (95% confidence interval: 1.3 to 27.3, p = 0.01). Of all patients having an MI between 12 am and 6 am, 91% had OSA. CONCLUSIONS: The diurnal variation in the onset of MI in OSA patients is strikingly different from the diurnal variation in non-OSA patients. Patients with nocturnal onset of MI have a high likelihood of having OSA. These findings suggest that OSA may be a trigger for MI. Patients having nocturnal onset of MI should be evaluated for OSA, and future research should address the effects of OSA therapy for prevention of nocturnal cardiac events