Correspondence to Dr Arshad A Khan; [email protected]
Strengths and limitations of this study
This study enrolled ST-segment elevation myocardial infarction patients undergoing primary percutaneous coronary intervention with current generation stents/advanced pharmacotherapy.
The study’s prospective design is a key strength.
The study is set in a single centre and had a relatively small sample size.
We did not calculate GRACE/Syntax score for our cohort.
Introduction
Adverse myocardial remodelling due to ST-segment elevation myocardial infarction (STEMI) is a significant global health problem, with STEMI affecting both left ventricular systolic and diastolic function.1 The prognostic implications of reduced left ventricular ejection fraction (LVEF) in STEMI are already well established2 3; and the role of diastolic indices, including left ventricular end diastolic pressure (LVEDP), is of ongoing clinical and research interest.4–6 LVEDP, which reflects global left ventricular compliance, is easily measured during left heart catheterisation at the time of primary percutaneous coronary intervention (PCI).7 Elevated LVEDP in STEMI has been studied in the thrombolysis era and early in the primary PCI era in retrospective post hoc analyses and has been shown to be a predictor of death and heart failure; however, these cohorts are over 10 years old.8–11
The aim of the current analysis is to assess the prognostic value of an elevated LVEDP in STEMI patients undergoing primary PCI in current contemporary practice with second-generation stents, advanced evidence-based therapy for heart failure with reduced ejection fraction, and potent antiplatelet agents.
Methods
The Hunter LVEDP Study is a prospective, single-centre study enrolling STEMI patients undergoing primary PCI at John Hunter Hospital, Newcastle Australia over a 5-year period from 1 January 2015 to 31 December 2019. All patients had primary PCI with a focus on door to balloon time, followed by guideline-directed medical therapy. The practice of checking LVEDP and performing left ventriculogram after primary PCI is variable and operator dependent, not being standard practice at this stage.7 There were 7 operators performing procedures during the study period with median experience of 15 years (range: 5 to 27 years). The LVEDP is adjudicated on the left ventricular pressure tracing at end expiration just prior to isovolumetric contraction and immediately after the ‘a’ wave at a point that corresponds to the ‘R’ wave of the ECG tracing.12
The primary endpoint in the present analysis is the combination of 12-month all-cause mortality and heart failure admissions, comparing different quartiles of LVEDP.
We used the Shapiro-Wilk test to assess normality of distribution of the data. Continuous variables are presented as mean±SD and compared using t-tests. Non-parametric variables are presented as median and IQR. Categorical variables are presented as number/per cent and compared using χ² test. Kaplan–Meier methods were used to estimate event rates at follow-up and to plot time-to-event curves; comparisons were made using the log-rank test. Univariate and multivariate Cox regression models were used to model the outcomes of death and heart failure using LVEDP as a categorical variable that is, quartiles.
All statistical analyses were programmed using STATA and SAS v9.4 (SAS Institute, Cary, North Carolina, USA). Our study was approved by the Hunter New England health ethics review committee (HNEHREC Reference No: 17/08/16/5.12).
Patient and public involvement
None.
Results
A total of 997 patients underwent primary PCI at our hospital during the study period (age: 64±13 years, males: 73%; n=728). The proportion with anterior STEMI was 42% (n=417). The LVEDP was measured during primary PCI in 590 (59%) patients. The LVEDP-measured patients were younger (63±13 vs 65±13 years, p=0.05), and more likely to be males (n=448, 76% vs n=277, 68%, p=0.01), with a higher incidence of anterior STEMI (n=271, 46% vs n=155, 38%, p=0.01). A total of 939 patients (94%) had drug-eluting stents. The mean total ischaemic and door to balloon times were 246±112 and 86±37 min respectively. A total of 938 (94%) patients had at least 1 stent inserted during the procedure. The drug-eluting stents were used in 95% of patients (n=891).
There was no difference in LVEF (measured with transthoracic echocardiogram during index hospitalisation), incidence of cardiogenic shock, out of hospital cardiac arrest or intra-aortic balloon pump use between those who did and did not have LVEDP measured. The 30-day all-cause mortality in patients with and without LVEDP measured was 4% vs 6.6%, p=0.05; the respective values for 12-month all-cause mortality were 6.4% vs 11.5%, p=<0.01 respectively. The mean LVEF for the whole cohort was 50%.
The median LVEDP for the whole cohort was 27 mm Hg (IQR: 22–31 mm Hg). When divided into quartiles, the median LVEDP was 17 mm Hg (IQR: 13–18 mm Hg) and 33 mm Hg (IQR: 30–36 mm Hg) in the 1st and 4th quartiles respectively (p<0.01). The baseline characteristics of all quartiles are demonstrated in table 1. At 30 days, all-cause mortality was 2% and 10% (p=0.001) in 1st and 4th quartiles respectively. At 1 year, the composite endpoint of all-cause mortality or heart failure admission was 12% vs 26% (p=0.01) in quartiles 1 and 4 respectively (table 2 and figure 1). In multivariate regression analysis, age, anterior STEMI, out of hospital cardiac arrest and LVEDP quartile 4 were independent predictors of mortality; whereas, LVEF dropped out of the model. None of the patients had coronary artery perforation.
Enlarge this image.Figure 1. Long-term Kaplan-Meier survival curve showing early separation of quartile 4 that is, highest left ventricular end-diastolic pressure quartile had worse prognosis.
Baseline characteristics of whole cohorts and LVEDP quartiles
| Demographics | All (n=997) | LVEDP quartile 1 (n=173) | LVEDP quartile 2 (n=123) | LVEDP quartile 3 (n=160) | LVEDP quartile 4 (n=134) | P value |
| LVEDP (mm Hg) – median (IQR) | 24 (13–36) | 17 (13–18) | 22 (20–22) | 26 (25–28) | 33 (30–36) | <0.01 |
| Age (years) – mean (SD) | 64 (13) | 63 (13) | 62 (12) | 64 (13) | 64 (14) | 0.8 |
| Males – n (%) | 724 (72) | 133 (77) | 100 (81) | 120 (75) | 96 (72) | 0.3 |
| ATSI – n (%) | 24 (5) | 8 (5) | 2 (2) | 6 (4) | 3 (2) | 0.4 |
| BMI (kg/sq m) – mean (SD) | 29 (5) | 30 (5) | 29 (4) | 29 (4) | 29 (5) | 0.7 |
| Procedural characteristics | ||||||
| Anterior MI – n (%) | 417 (42) | 62 (36) | 47 (38) | 82 (51) | 79 (59) | 0.01 |
| Systolic BP (mm Hg) – mean (SD) | 131 (22) | 131 (19) | 131 (21) | 133 (22) | 131 (22) | 0.9 |
| Diastolic BP (mm Hg) – mean (SD) | 77 (14) | 76 (13) | 78 (14) | 79 (13) | 78 (14) | 0.5 |
| OOHCA – n (%) | 65 (7) | 8 (5) | 5 (4) | 11 (7) | 11 (8) | 0.2 |
| Cardiogenic shock – n (%) | 82 (8) | 9 (5) | 6 (5) | 11 (7) | 18 (13) | 0.05 |
| IABP use – n (%) | 20 (2) | 1 (1) | 0 | 3 (2) | 6 (4) | 0.1 |
| Stent diameter (mm) – mean (SD) | 3 (0.6) | 3.2 (0.6) | 3.2 (0.5) | 3.0 (0.5) | 3.2 (0.6) | 0.9 |
| Stent length (mm) – median (IQR) | 22 (11) | 23 (12) | 23 (13) | 23 (11) | 23 (12) | 0.9 |
| TIMI III flow post procedure – n (%) | 929 (93) | 171 (99) | 118 (96) | 153 (96) | 127 (95) | 0.6 |
| Prior MI – n (%) | 164 (17) | 33 (19) | 14 (11) | 26 (16) | 30 (22) | 0.3 |
| Prior PCI – n (%) | 107 (11) | 21 (12) | 13 (11) | 17 (11) | 17 (13) | 0.7 |
| Prior CABG – n (%) | 35 (4) | 6 (3) | 2 (2) | 4 (3) | 5 (4) | 0.7 |
| DM – n (%) | 213 (22) | 38 (22) | 21 (17) | 38 (24) | 32 (24) | 0.8 |
| HTN – n (%) | 545 (55) | 113 (65) | 59 (48) | 71 (44) | 82 (61) | 1.0 |
| Dyslipidaemia – n (%) | 352 (36) | 67 (39) | 36 (29) | 44 (28) | 47 (35) | 0.3 |
| Smoking – n (%) | 415 (42) | 82 (47) | 57 (46) | 72 (45) | 55 (41) | 0.09 |
| Baseline haemoglobin (g/L) – median (IQR) | 138 (125–151) | 139 (117–148) | 140 (124–150) | 140 (123–147) | 136 (121–150) | 0.8 |
| Creatinine (micromole/L) – median (IQR) | 82 (71–99) | 89 (73–97) | 88 (80–98) | 86 (74–99) | 94 (83–101) | 0.2 |
| Peak troponin (ng/L) – median (IQR) | 36 (13–87) | 48 (13-87) | 57 (11–77) | 59 (34–69) | 89 (56–100) | 0.4 |
| LVEF (%) – mean (SD) | 50 (10) | 53 (11) | 52 (13) | 51 (10) | 47 (11) | 0.2 |
| PASP (mm Hg) – median (IQR) | 35 (28–42) | 37 (29–43) | 33 (24–39) | 34 (28–43) | 39 (31–49) | 0.3 |
| E/E′ ratio – mean (SD) | 11 (4) | 11 (4) | 10 (3) | 11 (4) | 12 (5) | 0.9 |
| Medications | ||||||
| ACEi – n (%) | 260 (27) | 61 (35) | 24 (20) | 29 (18) | 41 (31) | 0.8 |
| BB – n (%) | 96 (10) | 19 (11) | 7 (6) | 10 (6) | 16 (12) | 0.5 |
Only patients with LVEDP-measured are included in the analysis.
ACEi, ACE converting enzyme inhibitor; ATSI, Aboriginal and/or Torres Strait Islander; BB, beta blockers; BMI, Body Mass Index; BP, blood pressure; CABG, coronary artery bypass grafting; DM, diabetes mellitus; HTN, hypertension; IABP, intra-aortic balloon pump; LVEDP, left ventricular end diastolic pressure; LVEF, left ventricular ejection fraction; MI, myocardial infarction; n, number; OOHCA, out of hospital cardiac arrest; PASP, pulmonary artery systolic pressure; PCI, percutaneous coronary infraction; STEMI, ST-segment elevation myocardial infarction; TIMI, thrombolysis in myocardial infarction.
Table 2Outcomes and LVEDP quartiles (1 year)
| Quartile 1 (n=173) | Quartile 2 (n=123) | Quartile 3 (n=160) | Quartile 4 (n=134) | P value | |
| LVEDP (mm Hg) – median (IQR) | 17 (13–18) | 22 (20–22) | 26 (25–28 | 33 (30–36) | <0.01 |
| Death or heart failure admissions – n (%) | 21 (12) | 11 (9) | 14 (9) | 35 (26) | <0.01 |
| HF admissions – n (%) | 13 (8) | 7 (6) | 8 (5) | 15 (11) | 0.2 |
| ACS – n (%) | 15 (9) | 17 (14) | 20 (13) | 21 (16) | 0.3 |
| Stroke – n (%) | 2 (1) | 1 (1) | 2 (1) | 3 (2) | 0.6 |
| Cardiac re-admissions – n (%) | 39 (23) | 31 (25) | 38 (24) | 35 (26) | 0.9 |
| All-cause mortality – n (%) | 8 (5) | 4 (3) | 6 (4) | 20 (15) | <0.01 |
ACS, acute coronary syndrome; HF, heart failure; LVEDP, left ventricular end-diastolic pressure; n, number.
Clopidogrel was the preferred second antiplatelet agent and (n=924, 93%). A total of 291 (30%) patients had periprocedural abciximab bolus/infusion administered. Radial artery was vascular access of choice (n=853, 86%). There was no incidence of coronary artery perforation.
Discussion
The Hunter LVEDP Study found that LVEDP is an independent predictor of mortality in STEMI patients undergoing primary PCI. The fact that the anterior STEMI with larger myocardium at risk/high ischaemic burden and highest LVEDP quartile had worse prognosis/mortality is consistent with other observational studies.8 These results raise the question of whether early assessment and intervention to reduce LVEDP might favourably affect left ventricular remodelling (LVR) and improve clinical outcomes. Similarly, the prognostic implications of LVEDP in STEMI along with the index of microcirculatory resistance (IMR) and its additive utility with other haemodynamic parameters including systolic blood pressure and LVEF are a topic of ongoing research as well.13 Certainly, the patients with elevated LVEDP and IMR will be in the highest risk group.
Current major society guidelines focus on routine measurement of LVEF post STEMI at baseline and during follow-up, due to widely available expertise and non-invasive investigations.14 The known non-invasive diastolic parameters involving echocardiography have only a modest correlation with invasive haemodynamic measurements/LVEDP.15–17 Our cohort has relatively preserved LVEF (mean=50%). It is also the largest reported cohort in patients undergoing primary PCI with current generation stents. Our study shows that additional prognostic information can be obtained with LVEDP measurement in acute settings post primary PCI. Thus, measuring both LVEDP and LVEF can help predict outcomes after successful PCI for STEMI and could facilitate risk stratification, as it predicts LVR.18
The real-world practice of checking LVEDP is variable and left ventricular haemodynamics during primary PCI is not assessed universally. The higher all-cause mortality in patients without LVEDP measured, despite being younger and having no difference in LVEF, runs counter to the expected bias in observational studies (those with worse clinical presentation would likely have had more extensive investigations and more parameters measured); this needs further assessment in prospective studies. It is unclear if those patients had higher LVEDP or if other variables were responsible for the adverse prognosis.
The rationale for elevated LVEDP being a marker of worse prognosis is due to adverse LVR with subsequent left ventricular fibrosis and/or dilatation causing cardiomyopathy and ventricular arrhythmias. As per the Law of Laplace (left ventricular wall stress = (LVEDP × radius)/(2 × wall thickness), the LVEDP contributes to wall stress, which is the primary driver of LVR following STEMI.19 Thus, the interventions aimed at early reduction in LVEDP may reduce post STEMI LVR, heart failure and mortality. The possible explanation for worse prognosis with anterior STEMI is higher myocardium at risk.
In STEMI patients undergoing primary PCI, a few haemodynamic risk stratification models have been proposed. LVEDP, when used in conjunction with other parameters including LVEF, helps with prognostication in these models. Sola et al, in their retrospective analysis of 219 STEMI patients undergoing primary PCI, demonstrated that a systolic blood pressure to LVEDP ratio ≤4 predicted higher in-hospital mortality.20 Similarly, Ndrepepa et al, in an analysis of 1283 STEMI patients followed up for 8 years, demonstrated that a lower LVEF/LVEDP ratio was associated with increased risk of cardiac death.21 Similarly, in patients with acute coronary syndrome, the LVEF/LVEDP ratio, but not LVEF or LVEDP alone, improved predictive accuracy of multivariable models with respect to long-term cardiac mortality.22
The natural history of LVEDP in STEMI is not well understood.9 Although the management of myocardial infarction has advanced over the last few decades due to the availability of prehospital thrombolysis and/or timely primary PCI along with drug-eluting stents and pharmacotherapy for systolic heart failure, the mortality and morbidity from myocardial infarction are still substantial.23 Thus, early reduction of LVEDP, either pharmacologically or with mechanical therapies, may open another treatment target in patients with STEMI with the possibility of further reducing heart failure and mortality. Therefore, there is a need for adjunct cardio-protection and new approaches to limit myocardial infarct size and reduce progression to heart failure after STEMI.
LVEDP has seldom been used as a treatment target in myocardial infarction. Theoretically, the left ventricular unloading/reduction in LVEDP improves coronary perfusion thus limiting myocardial ischaemia and protects myocardial metabolism and mitochondrial function, which are key requirements for myocardial recovery after myocardial infarction.24 The elevated LVEDP in STEMI patients without cardiogenic shock can be safely reduced pharmacologically in the acute setting after primary PCI with a combination of nitrates and diuretics.25 Thus, it is enticing to speculate that the early reduction in LVEDP in myocardial infarction will reduce LVR and improve outcomes; however, this hypothesis remains to be tested in prospective randomised controlled trials, such as the ongoing Reduction of End Diastolic Pressure in Acute Myocardial Infarction (REDPAMI) trial (registered at ANZCTR.org.au; registration number ACTRN12618000096257).
The elevated LVEDP resulting in left ventricular loading correlates with the magnitude of myocardial injury in STEMI and has broad-reaching implications both for short and long-term clinical outcomes including adverse remodelling, heart failure and mortality.26 Similarly, recent studies report improved survival with left ventricular unloading with mechanical circulatory support in patients with and without cardiogenic shock.27 The proposed mechanism is venting the loaded ventricle. The door to unloading (DTU) trial is a contemporary study assessing left ventricular unloading in STEMI patients undergoing primary PCI.28 In this feasibility and safety study, 50 patients with anterior STEMI and elevated LVEDP were randomised to immediate reperfusion or 30 min of ventricular unloading with Impella Cardiac Power prior to reperfusion. It demonstrated the feasibility of Impella implantation before primary PCI and provided a signal of safety to allow for the development of a larger multicentre trial. A subanalysis of the DTU pilot trial showed that among patients with a larger area at risk, as determined by ST-segment sum elevation >6 mm, unloading for 30 min before reperfusion was associated with smaller infarct size compared with immediate reperfusion (44% vs 60%, respectively, p=0.04). This reinforces the hypothesis that patients with the largest area at risk, such as anterior STEMI, may receive the greatest benefit from an early left ventricular unloading approach.
Our study has important clinical implications being the first one from the current contemporary practice involving drug-eluting stents and timely provision of primary PCI. The use of drug-eluting stents has already demonstrated benefit in STEMI patients and addressing elevated LVEDP early will help outcomes further29—its limitations being relatively small sample size and lack of GRACE/Gensini/Syntax scores. Adding IMR could have added an extra dimension to our study, but it is unknown at this stage. Future haemodynamic studies with multicentre involvement and higher sample size will be helpful in studying this very important haemodynamic effect of STEMI care.
In conclusion, elevated LVEDP is an independent predictor of mortality in STEMI patients with relatively preserved LVEF. Future prospective studies are needed to assess the effects of early reduction in LVEDP on the clinical outcomes.
Data availability statement
Data are available upon reasonable request. Not applicable.
Ethics statements
Patient consent for publication
Consent obtained directly from patient(s).
Ethics approval
This study involves human participants and was approved by Hunter New England health ethics review committee (HNEHREC Reference No: 17/08/16/5.12). Participants gave informed consent to participate in the study before taking part.
X @arshadkhan129
Contributors AAK, AJB, TW, NC and JA contributed to study design, data analysis and manuscript writing. MSA-O, AAK, TW, MR and JT contributed to data collection and statistical analysis. AAK is responsible for the overall content as guarantor.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Not commissioned; externally peer reviewed.
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Details
; Williams, Trent 2 ; Ray, Max 3 ; Al-Omary, Mohammed S 4 ; Taylor, Jonah 4 ; Collins, Nicholas 5 ; Attia, John 6
; Boyle, Andrew J 7 1 Cardiovascular Department, John Hunter Hospital, New Lambton Heights, New South Wales, Australia; The University of Newcastle Australia, Callaghan, New South Wales, Australia
2 Cardiovascular Department, John Hunter Hospital, New Lambton Heights, New South Wales, Australia; School of Nursing and Midwifery, The University of Newcastle, Callaghan, New South Wales, Australia
3 Cardiovascular, Hunter New England Health, Newcastle, New South Wales, Australia
4 John Hunter Hospital, New Lambton Heights, New South Wales, Australia
5 Cardiology, John Hunter Hospital, Newcastle, New South Wales, Australia
6 Department of Medicine, University of Newcastle, Newcastle, New South Wales, Australia
7 The University of Newcastle Australia, Callaghan, New South Wales, Australia; John Hunter Hospital, New Lambton Heights, New South Wales, Australia