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

Login or register to view PDF.

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.

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


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.


  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.