Banded Versus Nonbanded Sleeve Gastrectomy: A Randomized Controlled Trial With 3 Years of Follow-up.

OBJECTIVE: The aim of this study was to compare silicone-banded sleeve gastrectomy (BSG) to nonbanded sleeve gastrectomy (SG) regarding weight loss, obesity-related comorbidities, and complications. SUMMARY BACKGROUND DATA: As a primary bariatric procedure, SG leads to excellent weight loss, yet weight regain is a relevant issue in mid- to long-term follow-up. Retrospective analyses suggest that banding a sleeve using a silicone ring may decrease weight regain and improve weight loss. METHODS: The banded versus nonbanded sleeve gastrectomy single-center, randomized controlled trial was conducted from January 2015 to August 2019. The primary endpoint was defined as excess weight loss 3 years after surgery. Secondary endpoints included the surgery's impact on obesity-related comorbidities, quality of life, and complications. The study was registered under DRKS00007729. RESULTS: Among 94 patients randomized, 97% completed 3-year follow-up. Mean initial body mass index was 50.9 kg/m [95% confidence interval (CI), 49.6-52.2]. Mean adjusted excess weight loss 3 years after SG amounted to 62.3% (95% CI, 56.2-68.5) and 73.9% ( 95% CI, 67.8-80.0) after BSG (difference 11.6%, P = 0.0073). Remission of type 2 diabetes occurred in 66.7% (4/6) after SG and in 91.0% (10/11) following BSG (P = 0.21). Three years after surgery, ring implantation correlated with decreased frequency of symptomatic reflux episodes (P = 0.01) but increased frequency of regurgitation (P = 0.03). The rate of major complications was not different between the study groups (BSG, n = 3; SG, n = 2; P = 0.63). Quality of life was better following BSG (P = 0.001). CONCLUSIONS: BSG provided better weight loss than nonbanded SG 3 years after surgery. Regurgitation was the main clinically relevant negative effect after BSG.

Effects of continuous positive airway pressure therapy on daytime and nighttime arterial blood pressure in patients with severe obstructive sleep apnea and endothelial dysfunction.

PURPOSE: A nocturnal non-dipping or rise in blood pressure (BP) is associated with poor cardiovascular outcome. This study aimed to test whether continuous positive airway pressure (CPAP) therapy can reduce nocturnal BP and normalize the 24-h BP profile in patients with severe obstructive sleep apnea (OSA) and erectile dysfunction as a surrogate for endothelial dysfunction (ED). PATIENTS AND METHODS: Eighteen consecutive patients with OSA and ED on stable antihypertensive medication (age 55.8 ± 9.5 years, body mass index 35.5 ± 3.8 kg/m2, apnea-hypopnoea index 66.1 ± 27.4/h) were treated with CPAP for 6 months (average daily use 5.8 ± 2.3 h). Twenty-four hour BP recordings were performed using a portable monitoring device. Rising was defined as an increase, whereas non-dipping was defined as a fall in nocturnal BP of less than 10% compared to daytime values. Serum noradrenaline levels as markers of sympathetic activity were measured at baseline and at 6 month follow up. RESULTS: Compared to baseline, nocturnal systolic and diastolic BP were significantly reduced after CPAP therapy (128.5 ± 14 to 122.9 ± 11 mmHg, p = 0.036; 76.2 ± 9 to 70.5 ± 5 mmHg, p = 0.007). The frequency of non-dipping and rising nocturnal systolic BP, as well as mean nocturnal heart rate, was reduced after CPAP treatment (73 to 27%, p = 0.039; 20 to 7%, p = 0.625; from 81.5 ± 10 to 74.8 ± 8 beats per minute p = 0.043). Serum levels of noradrenaline were significantly lower after CPAP therapy (398 ± 195 ng/l vs. 303 ± 135 ng/l, p = 0.032). CONCLUSION: In patients with severe OSA and clinically apparent ED, CPAP therapy was associated with a decrease in nocturnal BP and serum noradrenaline levels, as well as a normalization of the 24-h BP profile.

Sleep disordered breathing and enlargement of the right heart after myocardial infarction.

Structural and functional integrity of the right heart is important in the prognosis after acute myocardial infarction (AMI). The objective of this study was to assess the impact of sleep disordered breathing (SDB) on structure and function of the right heart early after AMI. 54 patients underwent cardiovascular magnetic resonance 3-5 days and 12 weeks after AMI, and were stratified according to the presence of SDB, defined as an apnoea-hypopnoea index of ≥ 15 events · h(-1). 12 weeks after AMI, end-diastolic volume of the right ventricle had increased significantly in patients with SDB (n=27) versus those without (n=25) (mean ± sd 14 ± 23% versus 0 ± 17%, p=0.020). Multivariable linear regression analysis accounting for age, sex, body mass index, smoking, left ventricular mass and left ventricular end-systolic volume showed that the apnoea-hypopnoea index was significantly associated with right ventricular end-diastolic volume (B-coefficient 0.315 (95% CI 0.013-0.617); p=0.041). From baseline to 12 weeks, right atrial diastolic area increased more in patients with SDB (2.9 ± 3.7 cm(2) versus 1.0 ± 2.4 cm(2), p=0.038; when adjusted for left ventricular end systolic volume, p=0.166). SDB diagnosed shortly after AMI predicts an increase of right ventricular end-diastolic volume and possibly right atrial area within the following 12 weeks. Thus, SDB may contribute to enlargement of the right heart after AMI.

Impact of sleep-disordered breathing on myocardial salvage and infarct size in patients with acute myocardial infarction.

AIMS: Sleep-disordered breathing (SDB) may be a risk factor for expansion of infarct size early after acute myocardial infarction (MI) by exposing the heart to repetitive oxygen desaturations and increased cardiac afterload. The objective of this study was to assess the impact of SDB on myocardial salvage and infarct size within 3 months after acute MI. METHODS AND RESULTS: Patients with acute MI and percutaneous coronary intervention were enrolled in this prospective observational study. All patients underwent cardiovascular magnetic resonance (CMR) to define salvaged myocardium and infarct size within three to five days and at 3 months after acute MI. Patients were stratified according to apnoea-hypopnoea index (AHI) assessed by polysomnography at baseline into those with (AHI ≥ 15/h) and without (AHI < 15/h) SDB. Of the 56 patients included, 29 (52%) had SDB. The area at risk between both groups was similar (40 ± 12% vs. 40 ± 14%, P = 0.925). Patients with SDB had significantly less salvaged myocardium (myocardial salvage index 52% vs. 77%, P < 0.001), smaller reduction in infarct size (0.3% vs. 6.5%, P < 0.001) within 3 months after acute MI, a larger final infarct size (23% vs. 12%, P < 0.001), and a lower final left ventricular ejection fraction (48% vs. 54%, P = 0.023). In a multivariate analysis, including established risk factors for large MI, AHI was independently associated with less myocardial salvage and a larger infarct size 3 months after acute MI. CONCLUSIONS: Sleep-disordered breathing was associated with less myocardial salvage and a smaller reduction in infarct size. These findings suggest a contribution of SDB to impaired healing of MI.

Natural course of sleep-disordered breathing after acute myocardial infarction.

The aim of this study was to test whether an improvement of left ventricular ejection fraction (EF) in the early phase after acute myocardial infarction is associated with a reduction of the severity of central and obstructive sleep apnoea. 40 consecutive patients with acute myocardial infarction underwent polysomnography and cardiovascular magnetic resonance imaging within 5 days and 12 weeks after the event to assess sleep apnoea and cardiac function. We stratified the sample in patients who improved their left ventricular EF within 12 weeks by ≥ 5% (improved EF group, ΔEF 9 ± 1%, n=16) and in those who did not (unchanged EF group, ΔEF -1 ± 1%, n=24). Prevalence of sleep apnoea (≥ 15 apnoea and hypopnoea events·h(-1)) within ≤ 5 days after myocardial infarction was 55%. Apnoea and hypopnoea events·h(-1) were significantly more reduced in the improved EF group compared with the unchanged EF group (-10 ± 3 versus 1 ± 3 events·h(-1); p=0.036). This reduction was based on a significant alleviation of obstructive events (-7 ± 2 versus 4 ± 3 events·h(-1); p=0.009), while the reduction of central events was similar between groups (p=0.906). An improvement of cardiac function early after myocardial infarction is associated with an alleviation of sleep apnoea. This finding suggests that re-evaluation of treatment indication for sleep apnoea is needed when a change in cardiac function occurs.

Obstructive sleep apnoea is associated with the development of diastolic dysfunction after myocardial infarction with preserved ejection fraction.

BACKGROUND: Left ventricular diastolic dysfunction is a predictor of adverse outcome after acute myocardial infarction (AMI). We aimed to test if sleep-disordered breathing (SDB) contributes to the development of diastolic dysfunction in patients with preserved left ventricular ejection fraction after AMI. METHOD: Patients with AMI, percutaneous coronary intervention and an ejection fraction ≥50% were included in this sub-analysis of a prospective observational study. Patients with AMI (n = 41) underwent cardiovascular magnetic resonance imaging (volume-time curve analysis) to define diastolic function by means of the normalised peak filling rate [nPFR; (end diastolic volume/second)]. In patients with AMI, the nPFR was assessed within <5 days and three months after AMI. Patients with AMI were stratified in patients with (apnoea-hypopnoea index, AHI ≥15/h) and without (AHI <15/h) SDB as assessed by polysomnography. RESULTS: At the time of AMI, the nPFR was similar between patients with and without SDB (2.90 ± 0.54 vs. 3.03 ± 1.20, p = 0.662). Within three months after AMI, diastolic function was significantly lower in patients with SDB than in patients without SDB (ΔnPFR: -0.83 ± 0.14 vs. 0.03 ± 0.14; p < 0.001; ANCOVA, adjusted for baseline nPFR). In contrast to central AHI, obstructive AHI was associated with a lower nPFR three months after AMI, after accounting for established risk factors for diastolic dysfunction [multiple linear regression analysis, B (95%CI): -0.036 (-0.063 to -0.009), p = 0.011]. CONCLUSION: Our data indicate that obstructive sleep apnoea impairs diastolic function early after myocardial infarction.

The impact of epicardial adipose tissue in patients with acute myocardial infarction.

AIMS: Epicardial adipose tissue (EAT) has been linked to impaired reperfusion success after percutaneous coronary intervention (PCI). Whether EAT predicts myocardial damage in the early phase after acute myocardial infarction (MI) is unclear. Therefore, we investigated whether EAT in patients with acute MI is associated with more microvascular obstruction (MVO), greater ST-deviation, larger infarct size and reduced myocardial salvage index (MSI). METHODS AND RESULTS: This retrospective analysis of a prospective observational study including patients with acute MI (n = 54) undergoing PCI and 12 healthy matched controls. EAT, infarct size and MSI were analyzed with cardiac magnetic resonance imaging, conducted 3-5 days and 12 weeks after MI. Patients with acute MI showed higher EAT volume than healthy controls (46 [25.;75. percentile: 37;59] vs. 24 [15;29] ml, p < 0.001). The high EAT group (above median) showed significantly more MVO (2.22 [0.00;5.38] vs. 0.0 [0.00;2.18] %, p = 0.004), greater ST-deviation (0.38 [0.22;0.55] vs. 0.15 [0.03;0.20] mV×10-1, p = 0.008), larger infarct size at 12 weeks (23 [17;29] vs. 10 [4;16] %, p < 0.001) and lower MSI (40 [37;54] vs. 66 [49;88] %, p < 0.001) after PCI than the low EAT group. After accounting for demographic characteristics, body-mass index, heart volume, infarct location, TIMI-flow grade as well as apnea-hypopnea index, EAT was associated with infarct size at 12 weeks (B = 0.38 [0.11;0.64], p = 0.006), but not with MSI. CONCLUSIONS: Patients with acute MI showed higher volume of EAT than healthy individuals. High EAT was linked to more MVO and greater ST-deviation. EAT was associated with infarct size, but not with MSI.

Obstructive sleep apnoea but not central sleep apnoea is associated with left ventricular remodelling after acute myocardial infarction.

OBEJCTIVE: Obstructive sleep apnoea (OSA) increases left ventricular transmural pressure more than central sleep apnoea (CSA) owing to negative intrathoracic pressure swings. We tested the hypothesis that the severity of OSA, and not CSA, is therefore associated with spheric cardiac remodelling after acute myocardial infarction. METHODS: This sub-analysis of a prospective observational study included 24 patients with acute myocardial infarction who underwent primary percutaneous coronary intervention. Spheric remodelling, calculated according to the sphericity index, was assessed by cardiac magnetic resonance imaging at baseline and 12 weeks after acute myocardial infarction. OSA and CSA [apnoea-hypopnoea index (AHI) ≥ 5/hour] were diagnosed by polysomnography. RESULTS: Within 12 weeks after acute myocardial infarction, patients with OSA exhibited a significant increase in systolic sphericity index compared to patients without sleep-disordered breathing (no SDB) and patients with CSA (OSA vs. CSA vs. no SDB: 0.05 ± 0.04 vs. 0.01 ± 0.04 vs. - 0.03 ± 0.03, p = 0.002). In contrast to CSA, the severity of OSA was associated with an increase in systolic sphericity index after accounting for TIMI-flow before percutaneous coronary intervention, infarct size, pain-to-balloon-time and systolic blood pressure [OSA: B (95% CI) 0.443 (0.021; 0.816), p = 0.040; CSA: 0.193 (- 0.134; 0.300), p = 0.385]. CONCLUSION: In contrast to CSA and no SDB, OSA is associated with spheric cardiac remodelling within the first 12 weeks after acute myocardial infarction. Data suggest that OSA-related negative intrathoracic pressure swings may contribute to this remodelling after acute myocardial infaction.

Rationale and design of the randomised Treatment of sleep apnoea Early After Myocardial infarction with Adaptive Servo-Ventilation trial (TEAM-ASV I).

AIMS: In acute myocardial infarction (AMI), impaired myocardial salvage and large infarct size result in residual heart failure, which is one of the most important predictors of morbidity and mortality after AMI. Sleep-disordered breathing (SDB) is associated with reduced myocardial salvage index (MSI) within the first 3 months after AMI. Adaptive servo-ventilation (ASV) can effectively treat both types of SDB (central and obstructive sleep apnoea). The Treatment of sleep apnoea Early After Myocardial infarction with Adaptive Servo-Ventilation trial (TEAM-ASV I) will investigate the effects of ASV therapy, added to percutaneous coronary intervention (PCI) and optimal medical management of AMI, on myocardial salvage after AMI. METHODS/DESIGN: TEAM ASV-I is a multicentre, randomised, parallel-group, open-label trial with blinded assessment of PCI outcomes. Patients with first AMI and successful PCI within 24 h after symptom onset and SDB (apnoea-hypopnoea index ≥ 15/h) will be randomised (1:1 ratio) to PCI and optimal medical therapy alone (control) or plus ASV (with stratification of randomisation by infarct location; left anterior descending (LAD) or no LAD lesion). The primary outcome is the MSI, assessed by cardiac magnetic resonance imaging. Key secondary outcomes are change of infarct size, left ventricular ejection fraction and B-type natriuretic peptide levels and disease-specific symptom burden at 12 weeks. CONCLUSION: TEAM ASV-I will help to determine whether treatment of SDB with ASV in the acute phase after myocardial infarction contributes to more myocardial salvage and healing. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02093377. Registered on March 21, 2014.

CPAP therapy improves erectile function in patients with severe obstructive sleep apnea.

OBJECTIVES: Erectile dysfunction (ED) is highly prevalent in obstructive sleep apnea (OSA), however, the effect of continuous positive airway pressure (CPAP) therapy on erectile function has not yet been thoroughly investigated in these patients. METHODS: Ninety-four men with severe OSA (ie, with an apnea-hypopnea-index ≥ 30/h of sleep) were prospectively evaluated for the presence and severity of ED before and after 6-12 months of CPAP therapy. The abbreviated version of the International Index of Erectile Function, (the IIEF-5) was used to rate erectile function. Furthermore, all study participants responded to standard questionnaires of daytime sleepiness (Epworth Sleepiness Scale), quality of life (WHO Wellbeing 5 questionnaire) and depression (Major Depression Inventory). RESULTS: ED as defined by an IIEF-5 score of ≤21 was present in 64 patients (68.1%). CPAP treatment significantly improved erectile function in those patients suffering from moderate and severe ED. Additionally, a trend for a correlation between the improvement of erectile function under CPAP and the hours of its use was observed. Finally, this effect was associated with larger improvements of quality of life in affected patients. CONCLUSIONS: ED is very frequent in men with severe OSA and can at least partly be reversed by long-term CPAP therapy in most seriously affected patients. The beneficial effect on erectile function may depend on CPAP compliance and is accompanied by improvements of quality of life. Randomized controlled trials are needed to confirm these findings.

[Sleep Apnea]. / Schlafapnoe.

In 2017 the German Sleep Society (Deutsche Gesellschaft für Schlafforschung und Schlafmedizin, DGSM) published the new S3 guideline "Nonrestorative Sleep/Sleep Disorders, chapter "Sleep-Related Breathing Disorders in Adults".Sleep apnea contributes to an increased morbidity and mortality in patients with cardiovascular diseases, e. g. coronary heart disease, heart failure and diabetes mellitus and is associated with an increased perioperative risk. It is also an important comorbidity in respiratory, neurologic and oncologic diseases. Treatment of sleep apnea can improve daytime sleepiness, quality of life und reduce blood pressure. In patients with atrial fibrillation, obstructive sleep apnea treatment should be optimized to improve treatment results. In addition to CPAP (continuous positive airway pressure) therapy and mandibular advancement devices, there are new therapies (e. g. hypoglossal nerve stimulation). Telemonitoring can help to improved therapy adherence. Nevertheless, in a current study CPAP could not prevent cardiovascular events in patients with moderate-to-severe obstructive sleep apnea and established cardiovascular disease. Patients with predominantly central sleep apnea and systolic hear failure (left ventricular ejection fraction ≤ 45 %) had an increased cardiovascular mortality when treated with adaptive servoventilation. Therefore, ASV is contraindicated in this small group of patients. Further studies are ongoing.

Erratum to: Resolution of ST deviation after myocardial infarction in patients with and without sleep-disordered breathing.

[This corrects the article DOI: 10.1007/s11818-018-0154-8.].

Association of sleep-disordered breathing and disturbed cardiac repolarization in patients with ST-segment elevation myocardial infarction.

OBJECTIVE: In patients with ST-segment elevation myocardial infarction (STEMI), disturbed cardiac repolarization before percutaneous coronary intervention (PCI) is a risk factor for malignant ventricular arrhythmia. We tested the hypothesis that sleep-disordered breathing (SDB) in patients with STEMI is associated with disturbed cardiac repolarization. METHODS: Thirty-three patients with STEMI who underwent PCI were prospectively enrolled. To assess cardiac repolarization, the heart-rate corrected interval from the peak of the T wave to the end of the T wave (TpTec) and QTc intervals were assessed with 12-lead electrocardiography before PCI, within 24 h after PCI, and 12 weeks after PCI. SDB defined as an apnea-hypopnea index (AHI) ≥15 per hour was diagnosed by polysomnography. RESULTS: Before PCI, patients with SDB had a significantly prolonged TpTec interval compared to patients without SDB (133 vs 104 ms, p = 0.035). Within 24 h after PCI, the TpTec interval was 107 vs 92 ms (p = 0.178). QTc intervals showed a similar pattern (pre-PCI: 443 vs 423 ms, p = 0.199; post-PCI: 458 vs 432 ms, p = 0.115). In multiple linear regression analyses, AHI was significantly associated with prolonged TpTec intervals (pre-PCI: B-coefficient = 1.11, 95% confidence interval (CI) 0.48-1.74, p = 0.001; post-PCI: B = 0.97, 95% CI 0.29-1.65, p = 0.007), prolonged QTc intervals (pre-PCI: B = 1.05, 95% CI 0.20-1.91, p = 0.018; post-PCI: B = 1.37, 95% CI 0.51-2.24, p = 0.003), and higher TpTe/QT-ratios (pre-PCI: B = 0.16, 95% CI 0.05-0.27, p = 0.007; post-PCI: B = 0.13, 95% CI < 0.01-0.25, p = 0.036), independent of known risk factors for cardiac arrhythmia. CONCLUSION: In patients with STEMI, SDB was significantly associated with disturbed cardiac repolarization before and after PCI, independent of known risk factors. These findings suggest that SDB may contribute to the risk of developing malignant ventricular arrhythmia.

Treatment of sleep apnea in chronic heart failure patients with auto-servo ventilation improves sleep fragmentation: a randomized controlled trial.

BACKGROUND: Impaired sleep efficiency is independently associated with worse prognosis in patients with chronic heart failure (CHF). Therefore, a test was conducted on whether auto-servo ventilation (ASV, biphasic positive airway pressure [BiPAP]-ASV, Philips Respironics) reduces sleep fragmentation and improves sleep efficiency in CHF patients with central sleep apnea (CSA) or obstructive sleep apnea (OSA). METHODS: In this multicenter, randomized, parallel group trial, a study was conducted on 63 CHF patients (age 64 ± 10 years; left ventricular ejection fraction 29 ± 7%) with CSA or OSA (apnea-hypopnea Index, AHI 47 ± 18/h; 46% CSA) referred to sleep laboratories of the four participating centers. Participants were randomized to either ASV (n = 32) or optimal medical treatment alone (control, n = 31). RESULTS: Polysomnography (PSG) and actigraphy at home (home) with centralized blinded scoring were obtained at baseline and 12 weeks. ASV significantly reduced sleep fragmentation (total arousal indexPSG: -16.4 ± 20.6 vs. -0.6 ± 13.2/h, p = 0.001; sleep fragmentation indexhome: -7.6 ± 15.6 versus 4.3 ± 13.9/h, p = 0.003, respectively) and significantly increased sleep efficiency assessed by actigraphy (SEhome) compared to controls (2.3 ± 10.1 vs. -2.1 ± 6.9%, p = 0.002). Effects of ASV on sleep fragmentation and efficiency were similar in patients suffering from OSA and CSA. CONCLUSIONS: At home, ASV treatment modestly improves sleep fragmentation as well as sleep efficiency in CHF patients having either CSA or OSA.

Adaptive servo-ventilation therapy of central sleep apnoea and its effect on sleep quality.

OBJECTIVES: Poor sleep quality is common in patients with chronic heart failure (CHF). This study tested the hypothesis that adaptive servo-ventilation (ASV) therapy in CHF patients whose central sleep apnoea (CSA) was not suppressed by continuous positive airway pressure (CPAP) (CPAP-non-responders) would improve sleep quality compared to CPAP-responders receiving ongoing CPAP therapy. METHODS: Eighty-two patients with CHF (65 ± 9 years, left ventricular ejection fraction 35 ± 16 %) and CSA [apnoea-hypopnoea index (AHI) ≥15/h] were retrospectively studied. Within an average of 47 days, patients were reevaluated on CPAP therapy and stratified according to their suppression of CSA: 34 were CPAP-non-responders switched to ASV therapy the following day and 48 were CPAP-responders who continued on CPAP therapy. Polysomnographic parameters were assessed in the diagnostic night and on the last night of PAP therapy (CPAP or ASV) before the patient was discharged with the final pressure settings. RESULTS: Compared with the CPAP group, the ASV group had significantly greater reductions from baseline in AHI (-37 ± 15/h vs -28 ± 18/h, p = 0.02), arousal index (-12.7 ± 13.6/h vs -6.8 ± 12.5/h, p = 0.04) and sleep stage N1 (-9 ± 14 % vs -2 ± 12 %, p = 0.03). In addition, the ASV group gained significantly more rapid eye movement (REM) sleep compared with the CPAP group (+5 ± 9 % vs +1 ± 9 %, p = 0.02). CONCLUSIONS: CPAP therapy is effective in reducing AHI in a significant proportion of CHF patients with reduced ejection fraction and CSA. Treatment of CSA with ASV in CHF patients reduces sleep fragmentation and improves sleep structure to a significantly greater extent than changes seen in responders to CPAP therapy.

Sleep-Disordered Breathing and Coronary Artery Disease.

Coronary artery disease (CAD) is one of the most frequent diseases in industrial nations. Despite significant advances in diagnosis and therapy, CAD and its long-term consequences are important contributors to morbidity and mortality. Therefore, in addition to management of traditional CAD risk factors, there are continued efforts to evaluate other factors and comorbidities that might contribute to the development and progression of CAD. One such factor is sleep-disordered breathing (SDB), which is characterized by repetitive apneas, arousals from sleep, and intermittent hypoxia. There is increasing evidence that SDB is a risk factor for CAD. In the early phase after myocardial infarction (MI) the heart might be in a vulnerable state sensitive to the negative consequences of SDB, including increased cardiac workload and endothelial dysfunction, which might ultimately lead to a mismatch between oxygen demand and supply. Despite successful percutaneous coronary intervention, patients with acute MI and SDB have prolonged myocardial ischemia, less salvaged myocardium, and impaired left and right ventricular remodelling compared with those without SDB, all of which predispose to heart failure. Suppression of SDB with positive airway pressure therapy in the early phase after MI is feasible. However, whether treatment of SDB with positive airway pressure will be an effective nonpharmacological treatment approach that will prevent the development of heart failure after MI remains to be determined and is the subject of current investigations.

Cardiac workload in patients with sleep-disordered breathing early after acute myocardial infarction.

BACKGROUND: Sleep-disordered breathing (SDB) may promote an increase in cardiac workload early after acute myocardial infarction (AMI). We tested the hypothesis that in the early phase after AMI, SDB is associated with increased 24-h arterial BP, heart rate (HR), and, thus, cardiac workload. METHODS: In this prospective study, 55 consecutive patients with AMI and subsequent percutaneous coronary intervention (78% men; mean age, 54 ± 10 y; mean BMI, 28.3 ± 3.6 kg/m²; mean left ventricular ejection fraction [LVEF], 47% ± 8%) underwent polysomnography and 24-h ambulatory BP and heart rate monitoring within 5 days after MI. Cardiac workload was calculated as systolic BP multiplied by HR. The presence of SDB was defined as ≥ 10 apneas and hypopneas per hour of sleep. RESULTS: Fifty-five percent of the patients had SDB, of which 40% was predominantly central in nature. Patients with SDB had higher 24-h HR and systolic and diastolic BP compared with those without SDB (115 vs 108 mm Hg, P = .029; 71 vs 67 mm Hg, P = .034; 69 vs 64 beats/min, P = .050, respectively). Use of antihypertensive medication and ß-receptor blockers was similar in both groups. In a multivariate linear regression analysis, SDB was significantly associated with an increased 24-h cardiac workload (ß-coefficient, 0.364; 95% CI, 0.071-0.657; P = .016), independently of age, sex, BMI, LVEF, and antihypertensive medication. CONCLUSION: Patients with AMI and SDB have significantly increased 24-h BP, HR, and cardiac workload. Treatment of SDB may be a valuable nonpharmacologic approach to lower cardiac workload in these patients.