Culprit Lesion Coronary Intervention Before Complete Angiography in ST-Elevation Myocardial Infarction: A Randomized Clinical Trial.

Importance: Rapid reperfusion during primary percutaneous coronary intervention (PCI) is associated with improved outcomes among patients with ST-elevation myocardial infarction (STEMI). Although attempts at reducing the time from STEMI diagnosis to arrival at the catheterization laboratory have been widely investigated, intraprocedural strategies aimed at reducing the time to reperfusion are lacking. Objective: To evaluate the effect of culprit lesion PCI before complete diagnostic coronary angiography (CAG) vs complete CAG followed by culprit lesion PCI on reperfusion times among patients with STEMI. Design, Setting, and Participants: This open-label, prospective, randomized clinical trial was conducted between April 1, 2021, and August 31, 2022, among patients admitted to a tertiary center in Jerusalem, Israel, with a diagnosis of STEMI undergoing primary PCI. All patients were followed up for 1 year. Analysis was on an intention-to-treat basis. Intervention: Patients were randomized in a 1:1 ratio to undergo either culprit lesion PCI before complete CAG or complete CAG followed by culprit lesion PCI. Main Outcomes and Measures: A needle-to-balloon time of 10 minutes or less. Results: A total of 216 patients were randomized, with 184 patients (mean [SD] age, 62.9 [12.2] years; 155 men [84.2%]) included in the final intention-to-treat analysis; 90 patients (48.9%) were randomized to undergo culprit lesion PCI before CAG, and 94 (51.1%) were randomized to undergo to CAG followed by PCI. Patients who underwent culprit lesion PCI before complete CAG had a shorter mean (SD) needle-to-balloon time (11.4 [5.9] vs 17.3 [13.3] minutes; P < .001). The primary outcome of a needle-to-balloon time of 10 minutes or less was achieved for 51.1% of patients (46 of 90) who underwent culprit lesion PCI before CAG and for 19.1% of patients (18 of 94) who underwent complete CAG followed by culprit lesion PCI (odds ratio, 4.4 [95% CI, 2.2-9.1]; P < .001). Rates of adverse events were similar between groups. In a subgroup analysis, the effect of culprit lesion PCI before complete CAG on the primary outcome was consistent. There were no differences in rates of in-hospital, 30-day, and 1-year all-cause mortality. Conclusions and Relevance: In this randomized clinical trial of patients with STEMI, culprit lesion PCI before complete CAG resulted in shorter reperfusion times. Larger trials are needed to validate these results and to evaluate the effect on clinical outcomes. Trial Registration: ClinicalTrials.gov Identifier: NCT05415085.

Prevalence, Predictors, and Outcomes of Patients With ST-Elevation Myocardial Infarction and Angiographically Significant Coronary Artery Disease of Non-Infarct-Related Artery.

Patients with ST-elevation myocardial infarction (STEMI) can present with angiographically significant coronary artery disease (CAD) of non-infarct-related artery (IRA) or with IRA-only CAD. This study aimed to evaluate the prevalence, predictors, and outcome of patients with STEMI and angiographically significant CAD of non-IRA. All consecutive patients with STEMI who underwent primary percutaneous coronary intervention between 2000 and 2020 were included. Angiographically significant CAD was defined as >50% stenosis of the left main coronary artery and/or >90% stenosis for all other coronary arteries. A total of 2,663 patients had IRA-only CAD (80.2%) and 657 had angiographically significant non-IRA CAD (19.8%). Independent predictors for non-IRA CAD were male gender (odds ratio [OR] 1.34, 95% confidence interval [CI] 1.05 to 1.70, p = 0.021), age >50 years (OR 1.45, 95% CI 1.11 to 1.91, p = 0.007), and diabetes mellitus (OR 1.56, 95% CI 1.29 to 1.9, p <0.001), whereas smoking (OR 0.83, 95% CI 0.68 to 0.99, p = 0.004) and family history of CAD (OR 0.78, 95% CI 0.62 to 0.98, p = 0.032) were found to be negatively associated with non-IRA CAD. In-hospital 30-day and 1- and 5-year all-cause mortality were higher in patients with non-IRA CAD compared with IRA-only CAD (5.8% vs 2.5%, 8.5% vs 3.3%, 18.4% vs 7.6% and 36.3% vs 20.3%, respectively; p for all <0.001). In conclusion, 20% of patients with STEMI had angiographically significant non-IRA CAD. Older age, male gender, and diabetes mellitus were independent predictors for non-IRA CAD, whereas smoking and family history of CAD predicted IRA-only CAD. The presence of non-IRA CAD was associated with higher short- and long-term all-cause mortality rates.

CoreValve Prosthesis Depth: What is the Optimal Measurement Target?

BACKGROUND AND AIM OF THE STUDY: A major drawback of the transcatheter aortic valve replacement (TAVR) procedure using the self-expandable Medtronic CoreValve (MCV) prosthesis is the high incidence of conduction disturbances and the need for postprocedural permanent pacemaker (PPM) implantation. The depth of prosthesis implantation may be an important contributing factor. The study aim was to determine the relationship between angiographic measurements of the MCV prosthesis depth and the occurrence of new conduction disturbances and need for PPM after TAVR. METHODS: A retrospective analysis was conducted of 157 consecutive patients who had undergone TAVR procedures with the MCV between 2009 and 2013. Patients with pre-existing pacemakers (n = 27) were excluded. Prosthesis depth was defined as the angiographic distance from the lowest part of the prosthesis to the base of the non-coronary cusp (NCcD) and the base of the left coronary cusp (LCcD). RESULTS: A 26 mm MCV was implanted in 50% of patients, and a 29 mm MCV in 38%. The rate of new ≥2nd degree atrioventricular block (AVB) after TAVR was 5%, and the incidence of new left ventricular bundle branch block (LBBB) was 23%. PPMs were implanted in 13 patients (10%) within 30 days after the procedure. Freedom from new ≥2nd degree AVB, LBBB and the need for PPM after TAVR was significantly higher among patients with NCcD <6 mm or LCcD <8 mm (90% and 89%, respectively) compared to patients with NCcD ≥6 mm or LCcD ≥8 mm (53% and 54%, respectively) (p <0.0001). CONCLUSIONS: Prosthesis depth, measured relative to either the NCcD or LCcD, strongly predicted the occurrence of conduction disturbances and the need for PPM following TAVR with the MCV prosthesis.

Preprocedure Anemia Management Decreases Transfusion Rates in Patients Undergoing Transcatheter Aortic Valve Implantation.

BACKGROUND: Periprocedural blood transfusions are associated with long-term mortality in patients undergoing transcatheter aortic valve implantation (TAVI). We sought to assess the impact of a preoperative blood conservation approach in treating anemia and preventing blood transfusions in patients undergoing TAVI. METHODS: Our cohort consisted of all patients evaluated in our structural heart clinic between January 1, 2012 and December 31, 2014. From March 2013, all anemic TAVI candidates were referred to the blood conservation clinic (BCC). We evaluated the effectiveness of the program to increase hemoglobin levels and to decrease the blood transfusion rates in the TAVI cohort. A multivariable logistic regression model was used to evaluate the association of being assessed by the BCC with receipt of a blood transfusion. RESULTS: The cohort included 239 patients, 62% of whom were anemic. Beginning in March 2013, 60 patients were evaluated in the BCC and treated with intravenous/oral iron or subcutaneous epoetin alfa, or both. Patients who underwent blood conservation had a significant increase in hemoglobin levels from 10.8 ± 1.1 g/dL to 11.8 ± 1.2 g/dL (P < 0.001). Implementation of the BCC was associated with a substantial decrease in the average blood transfusion rate from 33.3% before program initiation to 15.3% after implementation (P < 0.001). After adjusting for baseline hemoglobin values and comorbidities, being assessed at the BCC was strongly associated with a reduction in the need for transfusion (odds ratio, 0.28; 95% confidence interval, 0.11-0.69; P = 0.006). CONCLUSIONS: Preprocedural anemia management was successful in improving hemoglobin levels in anemic patients and in decreasing transfusion rates in TAVI.

Gender differences in the prevalence and treatment of coronary chronic total occlusions.

BACKGROUND: Gender differences exist in the presentation and outcomes of patients with coronary artery disease (CAD). Our study objective was to compare gender differences in prevalence, co-morbidities, and revascularization treatment in CAD patients with chronic total occlusions (CTOs). METHODS: A retrospective analysis using the Canadian Multicenter CTO Registry, which included 1,690 consecutive CTO patients identified at coronary angiography and a control group of 7,682 non-CTO patients. RESULTS: The prevalence of women in the CTO group was significantly lower compared to the control group (19% vs. 30%, P < 0.001). Within the overall CTO group, women were significantly older than men (70 ± 12 vs. 66 ± 11 years, P < 0.001) with more comorbidities, including hypertension and heart failure. Rates of PCI in the CTO group were similar between gender (10%), however, women with CTO were treated significantly less by CABG compared to men (19% vs. 27%, P = 0.003). Moreover, compared to male patients, significantly fewer women undergoing CABG had revascularization of the CTO artery (84% vs. 93%, P = 0.03). Multivariable analysis indicated that female gender (along with age, chronic renal failure, prior MI and cerebro-vascular disease) were independent predictors for not receiving CABG treatment for CTO. CONCLUSIONS: Female gender differences exist in CTO patients with both lower prevalence of CTOs at angiography and lower revascularization rates of CTOs by CABG. © 2015 Wiley Periodicals, Inc.

Distal coronary embolization following acute myocardial infarction increases early infarct size and late left ventricular wall thinning in a porcine model.

BACKGROUND: Distal coronary embolization (DCE) of thrombotic material occurs frequently during percutaneous interventions for acute myocardial infarction and can alter coronary flow grades. The significance of DCE on infarct size and myocardial function remains unsettled. The aims of this study were to evaluate the effects of DCE sufficient to cause no-reflow on infarct size, cardiac function and ventricular remodeling in a porcine acute myocardial infarction model. METHODS AND RESULTS: Female Yorkshire pigs underwent 60 min balloon occlusion of the left anterior descending coronary artery followed by reperfusion and injection of either microthrombi (prepared from autologous porcine blood) sufficient to cause no-reflow (DCE), or saline (control). Animals were sacrificed at 3 h (n = 5), 3 days (n = 20) or 6 weeks (n = 20) post-AMI. Cardiovascular magnetic resonance (CMR), serum troponin-I, and cardiac gelatinase (MMP) and survival kinase (Akt) activities were assessed. At 3d, DCE increased infarct size (CMR: 18.8% vs. 14.5%, p = 0.04; serum troponin-I: 13.3 vs. 6.9 ng/uL, p < 0.05) and MMP-2 activity levels (0.81 vs. 0.49, p = 0.002), with reduced activation of Akt (0.06 versus 0.26, p = 0.02). At 6 weeks, there were no differences in infarct size, ventricular volume or ejection fraction between the two groups, although infarct transmurality (70% vs. 57%, p< 0.04) and ventricular thinning (percent change in mid anteroseptal wall thickness:-25.6% vs. 0.7%, p = 0.03) were significantly increased in the DCE group. CONCLUSIONS: DCE increased early infarct size, but without affecting later infarct size, cardiac function or ventricular volumes. The significance of the later remodelling changes (ventricular thinning and transmurality) following DCE, possibly due to changes in MMP-2 activity and Akt activation, merits further study.

MitraClip for papillary muscle rupture in patient with cardiogenic shock.

We report the successful use of the MitraClip device (Abbott Vascular, Santa Clara, CA) in a 68-year-old man with posterolateral ST-elevation myocardial infarction complicated by papillary muscle rupture and cardiogenic shock.

Perlecan heparan sulfate proteoglycan is a critical determinant of angiogenesis in response to mouse hind-limb ischemia.

BACKGROUND: Perlecan is a heparan sulfate proteoglycan (HSPG) constituent of the extracellular matrix with roles in cell growth, differentiation, and angiogenesis. The role of the HS side chains in regulating in vivo angiogenesis after hind-limb ischemia is unknown. METHODS: Heparan sulfate (HS)-deficient perlecan (Hspg2(Δ3/Δ3)) mice (n = 35), containing normal perlecan core protein but deficient in HS side chains, and wild-type (n = 33) littermates underwent surgical induction of hind-limb ischemia. Laser Doppler perfusion imaging (LDPI) and contrast-enhanced ultrasonography (CEU) provided serial assessment of hind-limb perfusion. Harvested muscles underwent immunostaining for endothelial cell density (CD31), real-time reverse transcription polymerase chain reaction RT-PCR for vascular endothelial growth factor (VEGF) mRNA expression and western blot analysis for VEGF and fibroblast growth factor (FGF)2 protein expression at days 2 and 28. RESULTS: Serial LDPI showed significantly greater perfusion recovery in ischemic limbs of wild-type compared with Hspg2(Δ3/Δ3) mice. CEU showed that normalized microvascular perfusion was increased in wild-type compared with Hspg2(Δ3/Δ3) mice at day 28 (0.67 ± 0.12 vs 0.26 ± 0.08; P = 0.001). CD31-positive cell counts were significantly higher in wild-type compared with Hspg2(Δ3/Δ3) mice on day 28 (122 ± 30 cells vs 84 ± 34 cells per high-power field [HPF]; P < 0.05). Endogenous VEGF mRNA expression (P < 0.05) and VEGF protein expression (P < 0.002) were significantly decreased in the ischemic limbs of Hspg2(Δ3/Δ3) mice compared with wild-type mice at day 2 and day 28, respectively. FGF2 protein expression showed no significant differences. CONCLUSIONS: These results suggest that the HS side chains in perlecan are important mediators of the angiogenic response to ischemia through a mechanism that involves upregulation of VEGF expression.

Native coronary artery patency after coronary artery bypass surgery.

OBJECTIVES: The aim of the study was to determine native coronary artery patency 1 year after coronary artery bypass grafting and to identify clinical and angiographic predictors for the development of a chronic total occlusion (CTO). BACKGROUND: In contrast to the large body of information regarding graft patency, data regarding atherosclerosis progression and vessel patency in surgically bypassed native coronary arteries are less clear. METHODS: Of the 440 patients who underwent 1-year follow-up angiography as part of the multicenter RAPS (Radial Artery Patency Study), included in our study were 388 patients (88%) for whom angiograms were available for review. Angiograms were reviewed for native coronary artery patency in an independent blinded manner. RESULTS: On the pre-operative angiogram, CTO of at least 1 native coronary vessel was demonstrated in 240 patients (61.9%) having 305 occluded vessels. At 1 year after coronary artery bypass grafting, at least 1 new native coronary artery CTO occurred in 169 patients (43.6%). In 7.5% of patients, the native artery and the graft supplying that territory were both occluded. A new CTO was almost 5 times more likely to occur in coronary vessels with a pre-operative proximal stenosis >90% compared with vessels with proximal stenosis <90% (45.5% vs. 9.5%, respectively, p < 0.001). Patients with a new CTO had significantly more baseline Canadian Cardiovascular Society class 4 angina compared with patients without a new CTO. A new CTO was less likely to occur in the left anterior descending artery (18.4%), supplied by the left internal thoracic artery. When comparing radial artery and saphenous vein grafts, neither the type of graft nor graft patency had any association with native coronary artery occlusion. CONCLUSIONS: CTO of surgically bypassed coronary arteries 1 year after coronary artery bypass grafting is extremely common.

Heparan sulfate side chains have a critical role in the inhibitory effects of perlecan on vascular smooth muscle cell response to arterial injury.

Perlecan is a proteoglycan composed of a 470-kDa core protein linked to three heparan sulfate (HS) glycosaminoglycan chains. The intact proteoglycan inhibits the smooth muscle cell (SMC) response to vascular injury. Hspg2(Δ3/Δ3) (MΔ3/Δ3) mice produce a mutant perlecan lacking the HS side chains. The objective of this study was to determine differences between these two types of perlecan in modifying SMC activities to the arterial injury response, in order to define the specific role of the HS side chains. In vitro proliferative and migratory activities were compared in SMC isolated from MΔ3/Δ3 and wild-type mice. Proliferation of MΔ3/Δ3 SMC was 1.5× greater than in wild type (P < 0.001), increased by addition of growth factors, and showed a 42% greater migratory response than wild-type cells to PDGF-BB (P < 0.001). In MΔ3/Δ3 SMC adhesion to fibronectin, and collagen types I and IV was significantly greater than wild type. Addition of DRL-12582, an inducer of perlecan expression, decreased proliferation and migratory response to PDGF-BB stimulation in wild-type SMC compared with MΔ3/Δ3. In an in vivo carotid artery wire injury model, the medial thickness, medial area/lumen ratio, and macrophage infiltration were significantly increased in the MΔ3/Δ3 mice, indicating a prominent role of the HS side chain in limiting vascular injury response. Mutant perlecan that lacks HS side chains had a marked reduction in the inhibition of in vitro SMC function and the in vivo arterial response to injury, indicating the critical role of HS side chains in perlecan function in the vessel wall.

Relationship between initial treatment strategy and quality of life in patients with coronary chronic total occlusions.

AIMS: Our objective was to evaluate the relationship between coronary chronic total occlusion (CTO) treatment strategy and quality of life improvements. METHODS AND RESULTS: This multicentre prospective cohort study enrolled consecutive CTO patients undergoing a non-urgent coronary angiogram who completed the Seattle Angina Questionnaire (SAQ) and EQ-5D at baseline and at one year. Strategies were: i) medical therapy, ii) PCI to non-CTO, iii) PCI to CTO, and iv) CABG. Multivariable regression models compared quality of life changes over time among strategies, accounting for repeat measures per patient. In our cohort of 387 patients, 154 underwent medical therapy, 83 had PCI to the non-CTO artery, 104 underwent CABG, and 46 underwent PCI to the CTO. Medically treated patients had no improvement on any SAQ domains. Patients with revascularisation of the CTO territory with either PCI or CABG had significant improvements in the physical limitation (PCI to CTO 60.5-76.4; CABG 61.6-80.1; p<0.001), angina frequency (PCI to CTO 79.0-92.7; CABG 82.1-97.9; p<0.001), and disease perception (PCI to CTO 50.5-75.0; CABG 50.2-80.0; p<0.001) domains. In non-CTO PCI patients, improvement was restricted to the angina frequency (82.8-93.3; p<0.001), and disease perception (53.8-71.4; p<0.001) domains. CONCLUSIONS: CTO territory revascularisation was associated with quality of life improvements.

Evolution of right ventricular function post-acute ST elevation myocardial infarction.

PURPOSE: To characterize the evolution of right ventricular (RV) function post-myocardial infarction (MI), to describe the culprit vessel involved with RV injury and to assess the concordance between RV injury on magnetic resonance imaging (MRI) and RV infarct on electrocardiogram (EKG). MATERIALS AND METHODS: Thirty-one patients underwent cardiovascular magnetic resonance (CMR) examinations at three time frames post-ST elevation MI (STEMI). RESULTS: Of those with an initial normal scan, RV function did not significantly change over time (60.6 ± 6.3, 57.8 ± 6.0, 55.4 ± 5.7, P > 0.05). However, in those whose RVEF (RV ejection fraction) was initially low, it significantly increased from the first scan to the third scan (46.2 ± 3.6, 50 ± 6.6, 51.3 ± 5.2, P < 0.01). Post-hoc testing revealed a significant difference between the 48-hour and the 6-month scan, and between the 48-hour and the 3-week scan; however, there was no significant difference between the 3-week and 6-month scans. Interestingly, 23% of patients with low RVEF at baseline had the left anterior descending (LAD) as the culprit vessel. Only 15% of the low RVEF at baseline group were classified as having an RVMI by EKG criteria. CONCLUSIONS: The optimal timepoint to assess for RV injury via CMR may be 3 weeks post-acute MI. Standard EKG criteria may underestimate RV injury when compared to CMR.

Risk score model for predicting mortality in advanced heart failure patients followed in a heart failure clinic.

The prevalence of heart failure (HF) in the population is increasing, concomitant with high incidence of rehospitalizations and mortality. The aim of this study was to characterize a prognostic risk score model for patients with chronic HF. A total of 500 patients followed at the HF clinic were evaluated by clinical, functional, laboratory, imaging, and therapeutic variables that were correlated to mortality during a follow-up period of 25 months. Risk stratification was carried out by applying a risk score model based on multivariate analysis. Predictors correlated with mortality during follow-up were systolic blood pressure <110 mm Hg, male sex, age older than 70 years, 6-minute walk distance <300 m, lack of ß-blocker therapy, hyperuricemia (>7.5 mg/dL), hyponatremia, and prolonged QTc interval (>450 ms). Based on these variables, a risk score model (score 0-55) was established and included low risk, score <21 (9% mortality during 2-year follow-up); moderate risk, 21 to 29 (22%); high risk, 30 to 35 (35%), and very high risk: ≥36 points (62% 2-year mortality). The risk model had good discrimination ability (concordance index 0.75), which was better than the performance of the Seattle Heart Failure Model on our cohort (0.69). Simple noninvasive characteristics examined during the initial admission to the HF clinic can serve as prognostic markers for mortality and may help in the process of therapeutic decision-making in patients with HF.

Increased serum levels of oxidative stress are associated with hospital readmissions due to acute heart failure.

OBJECTIVES: Inflammation and serum oxidative stress (OS) are important components in heart failure (HF) deterioration. In this study we tested the hypothesis that an increase in patients' sera OS levels is associated with acute HF (AHF) readmissions. METHODS: Thirty consecutive patients (mean age 71 ± 10 years) admitted with AHF were included in the study. Serum OS in these patients was measured in-hospital and repeatedly after discharge over a period of 8 weeks of follow-up in which we reordered patients' HF readmissions. Of the 30 patients, 13 (43%) were readmitted (RAD group) and 17 (57%) did not require readmission (NRAD group). RESULTS: OS levels before discharge from the first hospital admission in the 2 groups were similar (p = 0.84 and p = 0.56, respectively). However, using repeated measures ANOVA, we found that the interaction between the time points and the 2 groups of patients (RAD and NRAD) was statistically significant (p = 0.037). It is important to note that OS serum levels were more predictive of HF readmissions than were repeated simultaneous serum measurements of NT-proBNP (p = 0.97). CONCLUSIONS: Increased OS levels in AHF patients, after they have been discharged from the hospital, are associated with higher HF readmission rates. In AHF, OS is a dynamic parameter associated with HF deterioration.

Mortality rates and modes of death in heart failure patients with reduced versus preserved systolic function.

BACKGROUND: There are conflicting reports regarding the characteristics and mortality rates of heart failure patients with preserved (HFPSF) vs. reduced systolic left ventricular function (SHF). METHODS: We evaluated the clinical profiles, mortality rates and modes of death in 481 consecutive symptomatic heart failure patients. In 317(66%) patients LVEF was <40% (SHF), and in 164(34%) LVEF≥40% (HFPSF). RESULTS: Compared to the HFPSF group, SHF patients were predominantly younger males with ischemic etiology and less cardiovascular comorbidities such as obesity, hypertension, diabetes mellitus and atrial fibrillation. Over a mean follow-up period of 2 years, 148(31%) patients died. Overall mortality was similar between the two groups: 53(32%) HFPSF patients and 95(30%) SHF patients died (p=0.6), even after adjusting for baseline variables, including age, gender and comorbidities (hazard ratio 1.09; 95% confidence interval 0.74-1.61; p=0.67). In contrast to the similar mortality rates, the modes of death were different. SHF patients had higher death rates due to pump failure compared to the HFPSF group {32/95(34%) vs. 9/53(17%) patients, p=0.03}. A trend towards higher rate of non-cardiac death was observed in HFPSF group {33/53(62%) patients vs. 45/95(47%) patients, respectively, p=0.08}. The prevalence of arrhythmic death was similar in both groups {17/95(18%) vs. 10/53(19%) patients, p=0.9}. CONCLUSIONS: Although the characteristics of HFPSF and SHF patients are distinctively different, the mortality rates are similar. The mode of death is different among the two groups of patients, as pump failure death is significantly higher in SHF patients, while non-cardiac mortality is more prevalent in HFPSF patients.

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.