Photoplethysmography as a single source for analysis of sleep-disordered breathing in patients with severe cardiovascular disease.

Sleep-disordered breathing and Cheyne-Stokes breathing are often not diagnosed, especially in cardiovascular patients. An automated system based on photoplethysmographic signals might provide a convenient screening and diagnostic solution for patient evaluation at home or in an ambulatory setting. We compared event detection and classification obtained by full polysomnography (the 'gold standard') and by an automated new algorithm system in 74 subjects. Each subject underwent overnight polysomnography, 60 in a hospital cardiology department and 14 while being tested for suspected sleep-disordered breathing in a sleep laboratory. The sleep-disordered breathing and Cheyne-Stokes breathing parameters measured by a new automated algorithm system correlated very well with the corresponding results obtained by full polysomnography. The sensitivity of the Cheyne-Stokes breathing detected from the system compared to full polysomnography was 92% [95% confidence interval (CI): 78.6-98.3%] and specificity 94% (95% CI: 81.3-99.3%). Comparison of the Apnea Hyponea Index with a cutoff level of 15 shows a sensitivity of 98% (95% CI: 87.1-99.6%) and specificity of 96% (95% CI: 79.8-99.3%). The detection of respiratory events showed agreement of approximately 80%. Regression and Bland-Altman plots revealed good agreement between the two methods. Relative to gold-standard polysomnography, the simply used automated system in this study yielded an acceptable analysis of sleep- and/or cardiac-related breathing disorders. Accordingly, and given the convenience and simplicity of its application, this system can be considered as a suitable platform for home and ambulatory screening and diagnosis of sleep-disordered breathing in patients with cardiovascular disease.

Long-term assessment of nocturnal Cheyne-Stokes respiration in patients with heart failure.

PURPOSE: Cheyne-Stokes respiration (CSR) is a known controversial prognostic marker in patients with heart failure (HF). Little is known, moreover, about the development and progress of CSR in such patients. The CSR progress over time may be indicative for clinical deterioration in patients with HF disease METHODS: Prospective cohort sleep studies, with algorithm-based analyses of continuously or periodically monitored changes over time using standard pulse oximeter. Home testing for 4 months of patients recruited from the cardiology department of a large community medical center in Haifa, Israel. A total of 36 patients, 31 men and five women, aged between 50 and 74 years, with symptomatic chronic HF. RESULTS: Out of the 36 patients, 15 (42%) patients were found to have CSR. The CSR cycle length was chosen as the characteristic parameter which determines the periodicity of the event and its length. Analyses of CSR cycle length and duration in the 15 patients showed changes over time in the length of the CSR event only in patient with New York Heart Association (NYHA) 4 classification. CONCLUSIONS: Nocturnal CSR in patients with HF show small variations over time in the prevalence or duration of the cycle length and could be a marker for entering stage 4 or deterioration in the NYHA class of HF patient. Moreover, it may take years for HF patients to develop CSR or to increase the length of the cycle length of existing CSR, if they develop it at all.

The Relationship Between Body Mass Index and In-Hospital Mortality in the Contemporary Era of an Acute Myocardial Infarction Management.

BACKGROUND: The association between body mass index (BMI) and clinical outcomes following an acute myocardial infarction (AMI) remains controversial. Our objective was to investigate the relationship between BMI and AMI presentation, in-hospital clinical course and mortality in the contemporary era of AMI management. METHODS: Patients, hospitalized for an AMI between October 2015 and December 2016, were identified in the National Inpatient Sample (NIS) database. Socio-demographic and clinical data, including BMI, were collected and outcomes, including length of stay and mortality, were analyzed. Patients were divided into 6 BMI (kg/m2) subgroups; under-weight (≤19), normal-weight (20-25), over-weight (26-30), obese I (31-35), obese II (36-39) and extremely obese (≥40). Multivariable logistic regression model was used to identify predictors of in-hospital mortality. Linear regression model was used to identify predictors of length of stay (LOS). RESULTS: An estimated total of 125,405 hospitalizations for an AMI across the US were analyzed. Compared to the other BMI subgroups, the under-weight, normal-weight and extremely obese groups presented with a non-ST segment elevation AMI (NSTEMI) more frequently and were less likely to undergo coronary revascularization. The data show a J-shaped relationship between BMI and study outcomes with lower mortality in patients with BMI over 25 compared to normal- and low-weight patients. In the multivariate regression model, BMI group was found to be an independent predictor of mortality. CONCLUSION: J-shaped relationship between BMI and mortality was documented in patients hospitalized for an AMI in the recent years. These findings confirm that the "obesity paradox" persists during the contemporary era of an AMI management.

The Relationship Between Body Mass Index and In-Hospital Mortality in Patients Following Coronary Artery Bypass Grafting Surgery.

Background: The association between Body Mass Index (BMI) and clinical outcomes following coronary artery bypass grafting (CABG) remains controversial. Our objective was to investigate the real-world relationship between BMI and in-hospital clinical course and mortality, in patients who underwent CABG. Methods: A sampled cohort of patients who underwent CABG between October 2015 and December 2016 was identified in the National Inpatient Sample (NIS) database. Outcomes of interest included in-hospital mortality, peri-procedural complications and length of stay. Patients were divided into 6 BMI (kg/m2) subgroups; (1) under-weight ≤19, (2) normal-weight 20-25, (3) over-weight 26-30, (4) obese I 31-35, (5) obese II 36-39, and (6) extremely obese ≥40. Multivariable logistic regression model was used to identify predictors of in-hospital mortality. Linear regression model was used to identify predictors of length of stay (LOS). Results: An estimated total of 48,710 hospitalizations for CABG across the U.S. were analyzed. The crude data showed a U-shaped relationship between BMI and study population outcomes with higher mortality and longer LOS in patients with BMI ≤ 19 kg/m2 and in patients with BMI ≥40 kg/m2 compared to patients with BMI 20-39 kg/m2. In the multivariable regression model, BMI subgroups of ≤19 kg/m2 and ≥40 kg/m2 were found to be independent predictors of mortality. Conclusions: A complex, U-shaped relationship between BMI and mortality was documented, confirming the "obesity paradox" in the real-world setting, in patients hospitalized for CABG.

Transition from chronic compensated to acute decompensated heart failure: pathophysiological insights obtained from continuous monitoring of intracardiac pressures.

BACKGROUND: Approximately half of all patients with chronic heart failure (HF) have a decreased ejection fraction (EF) (systolic HF [SHF]); the other half have HF with a normal EF (diastolic HF [DHF]). However, the underlying pathophysiological differences between DHF and SHF patients are incompletely defined. The purpose of this study was to use echocardiographic and implantable hemodynamic monitor data to examine the pathophysiology of chronic compensated and acute decompensated HF in SHF versus DHF patients. METHODS AND RESULTS: Patients were divided into 2 subgroups: 204 had EF <50% (SHF) and 70 had EF >or=50% (DHF). DHF patients had EF of 58+/-8%, end-diastolic dimension of 50+/-10 mm, estimated resting pulmonary artery diastolic pressure (ePAD) of 16+/-9 mm Hg, and diastolic distensibility index (ratio of ePAD to end-diastolic volume) of 0.11+/-0.06 mm Hg/mL. In contrast, SHF patients had EF of 24+/-10%, end-diastolic dimension of 68+/-11 mm, ePAD of 18+/-7 mm Hg, and diastolic distensibility index of 0.06+/-0.04 mm Hg/mL (P<0.05 versus DHF for all variables except ePAD). In SHF and DHF patients who developed acute decompensated HF, these events were associated with a significant increase in ePAD, from 17+/-7 to 22+/-7 mm Hg (P<0.05) in DHF and from 21+/-9 to 24+/-8 mm Hg (P<0.05) in SHF. As a group, patients who did not have acute decompensated HF events had no significant changes in ePAD. CONCLUSIONS: Significant structural and functional differences were found between patients with SHF and those with DHF; however, elevated diastolic pressures play a pivotal role in the underlying pathophysiology of chronic compensated and acute decompensated HF in both SHF and DHF.

Sudden cardiac arrest as the initial presentation for left ventricular noncompaction cardiomyopathy.

A 37-year-old man without a significant medical history had an out-of-hospital sudden cardiac arrest. A bystander started cardiopulmonary resuscitation, and emergency medical services arrived promptly, confirmed ventricular fibrillation, and restored sinus rhythm. An emergent coronary arteriogram was normal. Transthoracic echocardiography revealed a severely reduced left ventricular ejection fraction and suggested left ventricular noncompaction. The patient's heart failure with reduced ejection fraction was treated with carvedilol, lisinopril, and spironolactone, and after he was weaned from the ventilator he received an implantable cardioverter-defibrillator. The patient's identical twin was treated in the same fashion for a sudden cardiac arrest. Although many experts think that left ventricular noncompaction cardiomyopathy is a distinct nosological entity, others think that it is simply a dilated cardiomyopathy with unusually prominent left ventricular trabeculae.

Application of implantable hemodynamic monitoring in the management of patients with diastolic heart failure: a subgroup analysis of the COMPASS-HF trial.

BACKGROUND: Nearly half of all patients with chronic heart failure (HF) have a normal ejection fraction (EF), and abnormal diastolic function (ie, diastolic heart failure [DHF]). However, appropriate management of DHF patients remains a difficult and uncertain challenge. METHODS AND RESULTS: The Chronicle Offers Management to Patients with Advanced Signs and Symptoms of Heart Failure (COMPASS-HF) trial was designed to evaluate whether an implantable hemodynamic monitor (IHM) was safe and effective in reducing the number of heart failure-related events (HFRE) in patients with chronic HF. The current study presents data on a prespecified and planned subgroup analysis from the COMPASS-HF trial: 70 patients with an EF > or =50% (ie, DHF). As such, this represents a subgroup analysis of the COMPASS-HF Trial. DHF patients were randomized to IHM-guided care (treatment) vs. standard care (control) for 6 months. All 70 patients received optimal medical therapy, but the hemodynamic information from the IHM was used to guide patient management only in the treatment group. The HFRE rate in DHF patients randomized to treatment was 0.58 events/6 months compared with DHF patients randomized to control, which was 0.73 events/6 months; this represented a 20% nonsignificant reduction in the overall HFRE rate in the treatment group (95% CI = -46, 56, P = .66). There was a 29% nonsignificant reduction in the relative risk of a HF hospitalization in the DHF patients randomized to treatment compared with DHF patients randomized to control (95% CI = -69, 70, P = .43). CONCLUSIONS: The IHM was shown to be safe and was associated with a very low system-related and procedure-related complication rate in DHF patients. However, in this subgroup analysis limited to 70 DHF patients, the addition IHM-guided care did not significantly lower the rate of HFR events. The results of this subgroup analysis in DHF patients, for whom there are currently no proven, effective management strategies, will be used to design future studies defining the effects of IHM-guided care in patients with DHF.

Renal Sympathetic Denervation Protects the Failing Heart Via Inhibition of Neprilysin Activity in the Kidney.

BACKGROUND: Sustained sympathetic activation contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventricular (LV) dysfunction in heart failure (HF). OBJECTIVES: This study investigated the effects of radiofrequency renal nerve denervation (RF-RDN) on the pathobiology of HF and the interaction between the renal sympathetic nerves and natriuretic peptide (NP) metabolism. METHODS: Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were subjected to 45 min of coronary artery ligation and reperfusion for 12 weeks. At 4 weeks post-reperfusion, SHR and WKY underwent either bilateral RF-RDN or sham-RDN. RESULTS: Following RF-RDN in both strains, LV ejection fraction remained significantly above those levels in respective sham-RDN rats, and at the end of the 12-week study, rats in both strains had significantly reduced LV fibrosis and improved vascular function. RF-RDN therapy significantly improved vascular reactivity to endothelium-dependent and -independent vasodilators as well as vascular compliance in the setting of severe HF. Improvements in LV function were accompanied by significant elevations in circulating NP as compared to those associated with sham-RDN. Further investigation into the cause of increased circulating NP levels demonstrated that RF-RDN significantly inhibited renal neprilysin activity in SHR and WKY with HF. Likewise, chronic treatment with the beta1 antagonist bisoprolol inhibited renal neprilysin activity and increased circulation NP levels in WKY with HF. CONCLUSIONS: This study identifies a novel endogenous pathway by which the renal nerves participate in the degradation of cardioprotective NP. Furthermore, removal of the influence of the renal nerves on kidney function attenuates renal neprilysin activity, augments circulating NP levels, reduces myocardial fibrosis, and improves LV function in the setting of HF.

Is bridging to transplantation with a left ventricular assist device a risk factor for transplant coronary artery disease?

BACKGROUND: Left ventricular assist device (LVAD) support is associated with coagulopathy, bleeding, increased blood transfusion, and increased anti-HLA antibody production. Increased anti-HLA antibody production is associated with early transplant rejection, transplant coronary artery disease (CAD), and decreased post-transplant survival rates. We asked whether bridging to transplantation with an LVAD increases the risk of transplant CAD. METHODS: We reviewed data for all adults (>18 years old) who underwent heart transplantation at our institution between 1988 and 2000. After exclusion of transplant recipients who survived <3 years, we divided the remaining cohort into 2 groups: those bridged to transplantation with LVADs (mean duration of support, 149 +/- 107 days, n = 29) and those in United Network for Organ Sharing Status 1 bridged to transplantation without LVADs (controls, n = 86). We compared groups in terms of disease cause, age, sex, donor age, panel-reactive antibody testing, crossmatching, pre- and post-transplant cholesterol concentrations, diagnosis of diabetes mellitus or treated hypertension, infections, calcium channel blocker use, transplant rejection, ischemic time, cytomegalovirus infection, pre-transplant transfusion, and incidence of transplant CAD (defined as any coronary lesion identified by coronary angiography). We considered p < 0.05 to be significant. RESULTS: The bridged and control groups were similar in all respects except mean ischemic time (217 +/- 58 minutes vs 179 +/- 67 minutes, p = 0.007), post-transplant cholesterol concentration (212 +/- 55 mg/dl vs 171 +/- 66 mg/dl, p = 0.007), and pre-transplant transfusion incidence (100% vs 22%, p < 0.001). The incidence of transplant CAD was similar in both groups during a 3-year follow-up period (28% vs 17%, p = 0.238) and during total follow-up (34% vs 35%, p = 0.969). Multivariate logistic regression analysis identified cholesterol concentration at 1 year after transplantation as a significant predictor of CAD at 3 years after heart transplantation (p = 0.0029, odds ratio = 0.984). CONCLUSIONS: Bridging to transplantation with an LVAD does not increase the risk of transplant CAD. Nevertheless, aggressive prophylactic therapy to minimize potential risk factors for transplant CAD, such as increased cholesterol concentration, is warranted in all transplant recipients.

Left ventricular assist device therapy for end-stage congestive heart failure: from REMATCH to the future.

Therapy for patients with end-stage cardiomyopathy continues to evolve, but clearly it must now involve left ventricular assist device therapy as either bridge-to-transplantation or destination therapy. Patients who are selected for left ventricular assist device support must be able to undergo the surgical implantation procedure safely and avoid common complications such as right heart failure. Adequate patient selection is essential and can typically be accomplished using simple hemodynamic measures. As left ventricular assist device technology evolves, pulsatile devices will likely be replaced by their newer axial flow counterparts, which offer decided advantages. In the future, therapy for end-stage heart failure will involve aggressive use of mechanical assist device therapy and, as more patients are supported with these devices and the technology improves, this will become a burgeoning field for cardiologists and cardiovascular surgeons.

A successful anticoagulation protocol for the first HeartMate II implantation in the United States.

Bleeding and thrombus formation are common problems with life-threatening implications in patients receiving a left ventricular assist device. We describe the anticoagulation protocol for the 1st patient in the United States to undergo successful implantation of the HeartMate II left ventricular assist system.

Left ventricular free wall rupture in acute myocardial infarction: a case report and literature review.

We describe a case of subacute left ventricular free wall rupture during acute myocardial infarction in a 68-year-old man. The diagnosis was confirmed by echocardiography. The patient was supported by an intra-aortic balloon pump until the ruptured wall could be successfully repaired by suturing and gluing a pericardial patch over the defect and bypassing the left anterior descending coronary artery with a vein graft. This case demonstrates that left ventricular free wall rupture is not always fatal and that early diagnosis and institution of intra-aortic balloon pump support in such patients can allow successful bridging to definitive emergency surgical therapy.

Posttransplant off-pump coronary bypass and laser revascularization in a Jehovah's Witness.

A 57-year-old man, who had received a heart transplant 14 years earlier, underwent coronary artery bypass grafting and transmyocardial laser revascularization for left main, left anterior descending, and circumflex coronary artery disease. The procedures were performed through a left thoracotomy incision without cardiopulmonary bypass. Because the patient was of the Jehovah's Witness faith, no blood or blood products were transfused.

Left ventricular assist device implantation in a patient with congenitally corrected transposition of the great arteries.

Congenitally corrected transposition of the great arteries (ccTGA) is a rare anomaly characterized by atrioventricular and ventriculo-arterial discordance and several other malformations that eventually lead to heart failure. We describe the case of a 53-year-old woman with ccTGA and aortic insufficiency who was a candidate for heart transplantation due to end-stage congestive heart failure. Her condition deteriorated before a suitable donor heart could be found; therefore, we placed a left ventricular assist device in the right (systemic) ventricle. Concomitantly, we removed the aortic (systemic) valve, closed the aortic annulus with a bovine pericardial patch, and repaired the mitral valve. The patient recovered uneventfully and was discharged from the hospital 2 months postoperatively. She underwent cardiac transplantation approximately 6 months later and continued to do well after 18 months.