Acute Change in Left Ventricle End-diastolic Pressure after Primary Percutaneous Coronary Intervention in Patients with ST Segment Elevation Myocardial Infarction


ST segment elevation myocardial infarction (STEMI) causes decreasing left ventricle compliance, increasing left ventricle end-diastolic pressure (LVEDP), and diastolic dysfunctioning. It is known that primary percutaneous coronary intervention (PCI) has an acute effect on left ventricle compliance. Aims: This study aims to determine whether left ventricle diastolic function improves and LVEDP decreases post-PCI in patients with STEMI. Methods:Twenty-nine patients (21 male, mean age 62±12) diagnosed with a first anterior or inferior STEMI and hospitalized in the first six hours were enrolled. Coronary angiography (CAG) showed occlusion of the right coronary artery (RCA), circumflex (Cx), or left anterior descending (LAD) coronary artery. Aortic pressure and LVEDP were measured and compared before and after PCI. Results: After successful reperfusion, left ventricle diastolic function improved and LVEDP decreased significantly. Decrease in mean LVEDP was 5.7±2.9mmHg (p=0.0005) and 4.9±6.5mmHg (p=0.026) in inferior and anterior MI, respectively. Clinical and electrocardiographic (ECG) findings improved quickly. Conclusion: Primary PCA provides rapid improvement of LVEDP and diastolic functions in both anterior and inferior MI. Left ventricular pressure (before and after PCI) can be measured during the procedure without any complication, so it can be used for quick evaluation of left ventricular diastolic function improvement. Keywords: percutaneous coronary intervention, acute myocardial infarction, measurement of left ventricle end-diastolic pressure.

Correspondence Details:Ömer Şatiroglu, MD, Rize Universitesi Tip Fakultesi Kardiyoloji bölümü, 53100, Rize, Turkey. E:

Copyright Statement:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

In acute myocardial infarction (MI), decreasing compliance of the left ventricle is directly associated with prognosis.1 In patients with ST segment elevation MI (STEMI), left ventricular filling pressure increases.2,3 Early improvement of perfusion after MI will improve left ventricle function and decrease the infarction area, thus decreasing mortality.4,5 The main goal of reperfusion treatment is not only to open epicardial vessels but also to improve cardiac cell and left ventricle function.6 The efficacy of reperfusion treatment may be shown indirectly with electrocardiography (ECG), by regression of ST elevation, but there is a need for methods to demonstrate left ventricle and microvascular function improvement.7–9 Primary percutaneous coronary intervention (PCI) is regarded as the best reperfusion model in STEMI. PCI may be used to show hemodynamic changes in the left ventricle or to measure left ventricle end-diastolic pressure (LVEDP) for evaluation of reperfusion efficacy and success.

In this study, we investigated the effect of reperfusion treatment on left ventricle function, measurement of left ventricle pressure, and changes in STEMI with PCI.

Materials and Methods

Twenty-nine patients (21 male, mean age 62±12 years) diagnosed with first anterior and inferior STEMI and hospitalized within six hours, and assigned to undergo PCI, were enrolled (see Table 1). Patients with cardiogenic shock, refractory ventricular arrhythmia, congestive heart insufficiency, previous MI history, advanced valve disease, or left ventricle thrombus were excluded. Before PCI, patients gave informed consent and the study was conducted in accordance with the Helsinki declaration and ethical rules.

Study Protocol

Prior to PCI, patients took aspirin, clopidogrel, and heparin. Cardiac thrombus and function of the left ventricle and valves were checked by echocardiography (VingMed Vivid 3 with 2.5MHz prop, GE Medical Systems, Hortan, Norway) in the intensive coronary unit. Patients were monitored.

Blood samples were taken for biochemistry, cardiac enzymes, and hemogram. Angiography was performed by standard Judkins method. A pigtail catheter was installed in the left ventricle via the femoral artery to measure aortic, left ventricle systolic, and end-diastolic pressure and measurements were recorded on a monitor (Philips Intellivue MP 20).

Measurement and Analysis of Left Ventricle Hemodynamics

Left ventricle pressure was recorded during PCI (before and after PCI, aortic pressure, left ventricle systolic pressure, and end-diastolic pressure) (see Figures 1 and 2). Coronary angiography and PCI were performed using the Philips Allura Exper Fd 10 (The Netherlands) with standard Judkins catheter. This procedure did not result in any time loss and PCI was completed in less than five minutes. PCI was completed in all patients without any complications. Pressure measurements were evaluated by taking into consideration hemodynamic variables, nitrate use, premature ventricular extrasystol, and arhythmias. Before and after PCI, aortic systolic pressure, aortic diastolic pressure, left ventricle end-diastolic pressure, and left ventricle systolic pressure were measured and recorded.

Statistical Analysis

Descriptive statistics results were presented as mean, standard deviation, median, minimum, and maximum; and number and percentage for numeric and categorical parameters, respectively. Differences between the groups for categorical parameters and non-parametrics were determined by X2 test and Fisher’s exact test, respectively. Measurements of left ventricular pressure before and after PCI were compared by t test. Statistical analysis was performed using SPSS v.15.0. Significance level was assumed as p<0.05.

Patient Demographics

The demographics of the 29 patients are shown in Table 1. On coronary angiography, 19 patients (64%) have right dominant system involvement. Mean time from starting symptoms to reperfusion was 5.35±1.12 hours and from hospitalization to primary PCI application was 44.12±19.2 minutes. Mean time from entering through the femoral artery to reperfusion was 14.2±1.3 minutes. There was no difference between patients with anterior and inferior MI in terms of sex, mean age, hypercholesterolemia, hypertension, family history of coronary artery disease (CAD), smoking, and diabetes.

Effects of Percutaneous Coronary Intervention on Left Ventricle Hemodynamics and Pressure

Table 2 shows LVEDPs and aortic pressures. It was observed that shortly after successful PCI reperfusion left ventricle diastolic functions improved and LVEDP decreased. Of 29 patients who underwent PCI because of acute STEMI, 28 developed Thrombolysis in MI (TIMI) grade 3 flow, and one had slow coronary flow (TIMI 2) because of micro embolus in the coronary artery. In the patient who developed slow coronary flow there was no change in LVEDP before and after PCI. Post-PCI LVEDP decreased in the other patients (see Figure 3). In these patients, clinical and ECG findings improved quickly. Decrease in EDP was significant in both patient groups with inferior and anterior MI (p<0.05). Decrease in LVEDP after PCI was the same in both patient groups with inferior and anterior MI. There was no statistically significant difference between the two groups (p=0.657). There was no statistically significant change before and after PCI for aortic systolic and diastolic pressures (p=0.868). Decrease in LVEDP without any change in systemic (aortic) pressure suggests that left ventricle compliance and left ventricle diastolic functions improved quickly after PCI.


The aim of acute MI treatment is to restore coronary circulation as soon as possible by opening the occluded vessel. Success of reperfusion treatment depends on time and rate of TIMI flow 3. However, recent studies reported that improvement in epicardial coronary artery circulation is not sufficient to show myocardial perfusion. The investigation of the efficacy of reperfusion treatment (thrombolytic or primary PCI), effects on left ventricle function (systolic and diastolic), and mortality requires different examinations and tools.10 These tools include regression of ST segment elevation in ECG and echocardiography monitoring of myocardial perfusion, coronary flow reserve (CFR) measurement after PCI, angiographic myocardial blush grade (MBG) analysis, corrected TIMI frame count (CTFC), and coronary flow rate by Doppler.7–9 The effects of primary PCI on left ventricle function in patients with acute MI may be determined by left ventricle pressure measured during PCI. In patients with acute STEMI, left ventricle compliance increases, left ventricle filling pressure/EDP decreases, and diastolic function improves after PCI. In the early period (in minutes), left ventricle systolic functions also increase partially.

Diastolic Function

In all STEMI studies, diastolic dysfunction was determined. Reperfusion improves passive diastolic features of the myocardium. Most previous findings were from experimental studies11,12 and they were evaluated after thrombolytic treatment.14 Primary PCI is the best reperfusion treatment and most previous PCI studies have echocardiography findings from the late period.13 In these studies there are no early changes in left ventricle function. Experimental and clinical studies have demonstrated that left ventricle compliance improves one week after reperfusion.14–16 Only one study showed early (in one hour) improvement of left ventricle diastolic function and decrease of LVEDP after PCI in patients with acute anterior MI.17 In our study we determined the improvement in both patient groups with anterior and inferior STEMI.

During elective PCI, the left ventricle pressure/volume curve has a positive change. Increased left ventricle filling pressure and diastolic function disturbances in stable angina pectoris improved rapidly post elective PCI and reperfusion.18,19 Left ventricle systolic function has no or minimal change in the early period of primary PCI. Studies that investigated thrombotic reperfusion treatment effects on left ventricle systolic function in STEMI patients demonstrated that minimal improvement was determined on left ventricle wall movement after one week.20

In our study, we determined that complete opening of the vessels that are responsible from MI resulted in a decrease of LVEDP in 10 minutes (see Figures 4–7). Post-PCI decrease of left ventricle diastolic filling pressure indicates the rapid improvement of left ventricle compliance and diastolic function. In these patients clinical symptoms improved rapidly after PCI. Without complication all patients were discharged in stable condition. After one-month follow-up, patients had no complaints or clinical symptoms.

During thrombolytic treatment, the effects of reperfusion may be recorded by echocardiography. However, it is not possible to evaluate left ventricle diastolic function during primary PCI.14 Recording left ventricle diastolic parameters and LVEDP in invasive conditions allows evaluation of PCI effects and results. LVEDP measurement did not result in any time loss or increased risk of complication.

Clinical Application

Acute MI prognostic factors include left ventricle systolic functional parameters.21 Nevertheless, diagnostic dysfunctions have come to prominence recently. In patients with acute MI and preserved systolic function, development of pulmonary congestion related to diastolic dysfunction and increased LVEDP is the marker of poor prognosis.22 In our study, LVEDP measurement during primary PCI allowed easy, rapid, and objective evaluation of diastolic function.


Primary PCI provides rapid improvement of LVEDP and diastolic functions in both anterior and inferior MI. Left ventricular pressure (before and after PCI) can be measured during the procedure without any complication, and so can be used for quick evaluation of left ventricular diastolic function improvement.


  1. Diamond G, Forrester JS, Effect of coronary artery disease and acute myocardial infarction on left ventricular compliance in man, Circulation, 1972;45:11–9.
  2. Bergstra A, Svilaas T, van Veldhuisen DJ, et al., Hemodynamic patterns in ST-segment elevation myocardial infarction: incidence and correlates of elevated filling pressures, Neth Heart J, 2007;75:95–9.
  3. Van Herck PL, Carlier SG, Claeys MJ, et al., Coronary microrascular dysfunction after myocardial infarction: increased coronary zero flow pressure both in the infarcted and in the remote myocardium is mainly related to lelt ventricular flling pressure, Heart, 2007;93:72314.
  4. Gruppo Italiano per 1o Studio della Streptochinasi nell’Infarto Miocardico (GISSI-I), Effectiveness of intravenous trombolytic treatment in acute myocardial infarction, Lancet, 1986;1:397–401.
  5. The GUSTO Angiographic Investigators, The effects of tissue plasminogen activator streptokinaze, or both on coronary artery patency, ventricular function and survival after acute myocardial infarction, N Engl J Med, 1993:329:1615–22.
  6. Andrews J, Straznicky IT, French JK, et al., ST-seqment recovery adds to the assessment of TIMI 2 and 3 flow in predicting infarct wall motion after trombolytic therapy, Circulation, 2000;101:2138–43.
  7. Suryapranata H, Zijlstra F, Macleod DC, et al., Predictive value of reactive hiperemic response on reperfusion on recover of regional myocardial function after coronary angioplasty in acute myocardial infarction, Circulation, 1994;89:1109–17.
  8. Greaves K, Dixon SR, Fejka M, et al., Myocardial contrast echocardiography is superior to other known modalities for assessing myocardial reperfusion after acute myocardial infarction, Heart, 2003;89:139–44.
  9. The TIMI 7 Study Group, The Thrombolisis In Myocardial Infarction (TIMI) trial, N Engl J Med, 1985;312:932–6.
  10. Zeymer U, Schröder R, Neuhaus KL, Patency, perfusion and prognosis in acute myocardial infarct, Herz, 1999;24:421–9.
  11. Lavallee M, Cox D, Patrick TA, Vatner SF, Salvage of myocardial function by coronary artery reperfusion 1, 2, and 3 hours after occlusion in conscious dogs, Circ Res, 1983;53:235–47.
  12. Raya TE, Gay RG, Lancister L, et al., Serial changes in left ventricular relaxation and chamber stifness after large myocardial infarction in rats, Circulation, 1988;77:1424–31.
  13. Cerisano G, Bolognese L, Canabba N, et al., Doppler-derived mitral deceleration time: an early strong predictor of left ventricular remodeling after reperfused anterior acute myocardial infarction, Circulation, 1999;99:230–6.
  14. Popovic A, Neskovic N, Marinkovic J, et al., Serial assessment of left ventricular chamber stiffness after acute myocardial infarction, Am J Cardiol, 1996;77:361–4.
  15. Forester JS, Diamond G, Parmley WW, Swan HJ, Early increase in left ventricular compliance after myocardial infarction, J Clin Invest, 1972;51:598–603.
  16. Williamson BD, Lim MJ, Buda AJ, Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction, Am J Cardiol, 1990;66:891–903.
  17. Remmelink M, Krischan D, Henriques PS, et al., Acute left ventricular dynamic effects of primary percutaneaus coronary intervention, J Am Coll Cardiol, 2009;53:1493–502.
  18. Kass DA, Midei M, BrinkerJ, Maughan WL, Influence of coronary occlusion during PTCA on end-systolic and end-diastolic pressure volume relations in humans, Circulation, 1990;81:442–60.
  19. Semrys PW, Wijns W, van den Brand M, et al., Left ventricular performance, regional blood flow, wall motion, and lactate metabolism during transluminal angioplasty, Circulation, 1984;70:25–36.
  20. Harrison JK, Califf RM, Woodlief LH, et al., For the TAMI Study Group. Systolic left ventricular function after reperfusion therapy for acute myocardial infarction. Analysis of determinants of improvement, Circulation, 1993;87:1537–47.
  21. Richards AM, Nicholls MG, Yantlle TG, et al., Plasma N-terminal pro-brain natriuretic peptide and adrenomedullin: new neurohormonal predictors of left ventricular function and prognosis after myocardial infarction, Circulation, 1999;97:1921–9.
  22. Moller JE, Pellikka PA, Hillis GS, Oh JK, Prognostic importance of diastolic function and filling pressure in patients with acute myocardial infarction, Circulation, 2006;114:438–44.