Skip to main content
Download PDF
Download ePub

Left ventricular diastolic dysfunction of the cardiac surgery patient; a point of view for the cardiac surgeon and cardio-anesthesiologist

Journal of Cardiothoracic Surgery volume 4, Article number: 67 (2009) Cite this article

Abstract

Background

Left ventricular diastolic dysfunction (DD) is defined as the inability of the ventricle to fill to a normal end-diastolic volume, both during exercise as well as at rest, while left atrial pressure does not exceed 12 mm Hg. We examined the concept of left ventricular diastolic dysfunction in a cardiac surgery setting.

Materials and methods

Literature review was carried out in order to identify the overall experience of an important and highly underestimated issue: the unexpected adverse outcome due to ventricular stiffness, following cardiac surgery.

Results

Although diverse group of patients for cardiac surgery could potentially affected from diastolic dysfunction, there are only few studies looking in to the impact of DD on the postoperative outcome; Trans-thoracic echo-cardiography (TTE) is the main stay for the diagnosis of DD. Intraoperative trans-oesophageal (TOE) adds to the management. Subgroups of DD can be defined with prognostic significance.

Conclusion

DD with elevated left ventricular end-diastolic pressure can predispose to increased perioperative mortality and morbidity. Furthermore, DD is often associated with systolic dysfunction, left ventricular hypertrophy or indeed pulmonary hypertension. When the diagnosis of DD is made, peri-operative attention to this group of patients becomes mandatory.

Peer Review reports

Introduction

Left ventricular diastolic dysfunction (DD) is defined as the inability of the ventricle to fill to a normal end-diastolic volume, both during exercise as well as at rest, while left atrial pressure does not exceed 12 mm Hg [1–3]. It has been shown that several patients with DD are suffering from paroxysmal dyspnoea and "unexplained" pulmonary oedema with a normal ejection fraction [4, 5]). Among patients operated for coronary artery disease or aortic stenosis, the incidence of left ventricular DD ranges widely between 44%, and 75% [6–10]. The significance and the severity of ventricular diastolic dysfunction among these patients are not well elucidated. On the other hand, estimation of the degree of DD peri-operatively, is difficult in up to 20% of cardiac-surgery patients for several reasons [10, 11] including rhythm abnormality, preload and afterload alterations, coexistence of valvular disease, age related changes, and inability to obtain proper Doppler images [12–15]. The diastolic heart failure annual mortality varies between 9-28% (four-fold that of disease-free subjects [16], while it has also been linked to increased incidence of postoperative complications (mortality or morbidity) after cardiac surgery [13, 17, 18]. Revascularization of ischemic myocardium seems to be beneficial for DD (if not immediately), some weeks after revascularization [19]. Potential direct postoperative improvement in diastolic function may be offset by the detrimental effect of global ischemia during cardioplegic arrest in combination with myocardial interstitial oedema [11, 20]. There are only a few studies concerning surgical outcomes of patients suffering from diastolic dysfunction. Moreover, intra-operative diagnosis and strategies to manage patients with left ventricular diastolic dysfunction are not well clarified. In that sense, diastolic dysfunction could be considered perioperatively as a "Trojan horse".

Source of Research

Pertinent medical literature in the English language was identified through a Medline computerized literature search and a manual search of selected articles using the key words "left ventricular diastolic dysfunction", "left ventricular diastolic impairment", "transmitral flow Doppler", "pulmonary venous flow patterns". The search terms were combined using the Boolean operator term "or" to find all abstracts pertaining to the chosen search terms. These individual terms were then combined using the Boolean operator term "and" to find articles that contained information of all search terms. The reference lists of articles found through these searches were also reviewed for relevant articles. Links provided on the web sites of published articles were searched for relevant articles.

Pathophysiology

DD is present when an elevated filling pressure is necessary to achieve normal ventricular filling. So, DD is related to abnormal left ventricular relaxation and filling during diastolic phase of cardiac cycle [21–24]. During this phase there are four timely and sequential events: a) isovolemic relaxation, b) rapid (early) LV filling, c) slow LV filling (diastasis) and d) atrial contraction [2, 23]. In figure 1 is shown schematically the pathophysiology of DD. According to echocardiographic depiction, filling of normally relaxed LV is completed in two phases: the first phase is due to the passive filling of the LV, is massive and depicted early in diastole by a high E wave. The second phase is due to the left atrial contraction, takes place during late diastolic phase, and leads to late LV filling depicted by the wave A of transmitral inflow Doppler [22, 25]. The rate of decrease of E wave in early diastole depends on the rate of increase in LV pressure and is represented by the so-called deceleration time (DT). This time is influenced by a number of factors such as, a) left atrial-left ventricular pressure gradient at the time of mitral valve opening, b) left atrial chamber compliance, c) left ventricular chamber compliance, d) grade of left ventricle relaxation, e) visco-elastic forces of the myocardial wall, f) pericardial restraint and finally g) left-right ventricular interaction. Left ventricular relaxation-similar to contraction- is an energy-dependent process, because it requires the re-uptake of calcium into the sarcoplasmic reticulum [26]. When patients with left ventricular DI are subjected to stress-as occurs during surgery or during faster heart rates-due to shorter diastolic filling time available, the ventricle is not allowed to relax and fill properly; thus, causing increased left ventricular end-diastolic pressure and pulmonary congestion [1, 2, 16]. Furthermore, relaxation of the left ventricle is determined by visco-elasticity and restoring forces (recoil). It is believed that impaired diastolic filling of the left ventricle is the first manifestation of active ischemia and results in an upward shift of left ventricular diastolic pressure-volume relationship [2, 26]. Decreased activity of sarcoplasmic reticulum calcium ATPase pump (SERCA) can slow down calcium removal out of the cytosolic net [27]. In contrast, increased levels or activity of phospholamban-the natural SERCA-inhibitory protein-can also impair relaxation. Hypothyroidism decreases SERCA and increases phospholamban, leading to impaired relaxation, while the opposite effect occurs in hyperthyroidism [27]. In a similar way, increasing the action of SERCA by administration of captopril, and β-agonists (or decreasing the action of phospholamban), results in improvement of diastolic relaxation [28].

Figure 1
figure 1

Pathophysiology of DD and its consequences.

Full size image

Pathophysiology and diagnosis of DD

Another aspect of DD is the relationship between systolic and diastolic left ventricular dysfunction [2, 29, 30] Increased left ventricular end systolic volume for example, affects the rate of left ventricular relaxation, and as a result, patients with reduced LV ejection fractions are expected to have a prolonged relaxation time [2]. Loading conditions, such as inotropic stimulation and neurohumoral factors generally affect both systolic and diastolic function in a parallel way [2]. As it has been shown, elevated left ventricular end-diastolic pressure may or may not be associated with systolic dysfunction of left ventricle, suggesting left ventricular DD even in the absence of reduced left ventricular ejection fraction [29]. Indeed, patients with symptoms of heart failure and normal ejection fraction have significant abnormalities in active relaxation and passive stiffness, which cause increased left ventricular end-diastolic pressure [30]. Literature review: "The theory" of DD is presented in table 1.

Table 1 Articles "investigating the background" of the entity Diastolic Heart Failure (DHF).
Full size table

Diagnosis of DD in a Cardiothoracic setting

Assessment and diagnosis of DD can be performed with non-invasive (2D and Doppler-echocardiography, colour Doppler M-mode, Doppler tissue imaging, MR-myocardial tagging, radionuclide ventriculography) and invasive techniques (micromanometry, angiography, conductance method). Typical findings of primary DD in chest radiograph include absence of cardiomegaly and presence of pulmonary congestion. Electrocardiogram/ECHO reveals the presence of excessive concentric hypertrophy in combination with normal ejection fraction [5]. Measurement of peak early filling wave (E wave: is caused by difference in atrium-ventricle pressure) and atrial filling wave (A wave: is caused by atrial contraction) ratio by Doppler echocardiography, as well as deceleration time (DT: is caused by left ventricular compliance), are useful screening tools for abnormal left ventricular relaxation [29]. In presence of abnormal relaxation, atrial contraction occurs in an incompletely empty atrium and blood is propelled into the left ventricle in increased velocity, accounting for the heightened A wave and consequent decreased E/A ratio. Blood flow in the pulmonary veins is biphasic, with peaks of forward flow occurring in both systole and diastole and inverse diastolic flow occurring during atrial contraction. There is an inverse relationship between left atrial pressure and pulmonary venous systolic flow. That is the reason why determination of systolic pulmonary venous flow velocity is a rapid method to estimate LV filling pressures after CABG [30].

Pathological filling is determined from transmitral flow pattern

  1. 1)

    Prolonged relaxation pattern: characterized by prolonged isovolumetric relaxation time and deceleration time, low E and high A wave velocities with an E/A wave ratio typically 1. It is related to the remodelling process including hypertrophy or scarring of an infarct zone leading to a non-uniform LV relaxation.

  2. 2)

    Pseudonormal pattern: an intermediate stage between prolonged relaxation and restrictive filling as a consequence of disease progression. There is an association with atrial dilatation and prominent pulmonary venous wave reversal.

  3. 3)

    Restrictive pattern: associated with shortened isovolumetric relaxation time, increased peak E wave velocity with very short deceleration time and small A wave, leading to an E/A wave ratio of 2. This pattern might be due to increasing LV volume and also to increased myocardial stiffness. DD is severe when the transmitral filling pattern E/A ratio is 2 and the deceleration time is 150 ms.

For patients undergoing cardiac surgery, Doppler assessment of transmitral flow has been used to estimate postoperative left ventricular filling pressure, relaxation, and stiffness [31]. The most important problem in evaluating transmitral flow patterns is their great variation, depending on many factors such as: heart rate [32, 33], preload [34], afterload [34], positive-pressure mechanical ventilation [21], systolic ventricular function [35, 36], use of inotropic or generally vasoactive agents due to their effect on the afterload [34, 37], and hemodilution (higher velocities due to reduced blood viscosity) [34]. To surmount this, a new method for diagnosis of LV diastolic dysfunction, the so called flow propagation velocity (Vp) is applied. It bears the advantage of being insensitive to heart rate and preload changes [10]. According to Vp measurement, left ventricular filling patterns does not change significantly after cardiopulmonary bypass. Furthermore, newer techniques such as tissue Doppler imaging (TDI) which measures high intensity, low velocity echo of the myocardium has been developed. By using TDI, local myocardial relaxation can be calculated by obtaining the velocity of early diastolic wall motion (Em) and it's timing [38]. In other words, TDI allows assessment of diastolic function because of its unique ability to assess regional abnormalities in relaxation, in addition to their global effect on ventricular relaxation and filling dynamics. An E/Em ratio > 10 remains the best discriminatory value when it is used as a single parameter for the prediction of elevated filling pressures or simply diastolic dysfunction [39]. However, definite diagnosis of diastolic dysfunction is established by cardiac catheterization and direct measurement of pressure at the end of systole and volume loops [40]. This invasive assessment of diastolic function allows the study of isovolumic relaxation (time constant of LV relaxation is longer > 50-55 msec) and evaluation of the passive elastic properties of the myocardium (LV passive-stiffness constant is high).

Intraoperative diagnosis

Intraoperative diagnosis of diastolic dysfunction is difficult, [41, 42] because: a) most variables measuring diastolic function depend on loading conditions, heart rate and age [32–34, 43], b) no single individual measurement can fully characterize left ventricular diastolic dysfunction, and c) ECHO estimation may give different results whether it is performed with the patient awake and breathing spontaneously, or anesthetized and receiving positive pressure ventilation [35]. Diastolic dysfunction of left ventricle can be intraoperatively diagnosed, estimated and graded by using Trans Oesophageal Echo (TOE). Moreover, valuable information may be obtained with the additional use of a Swan-Ganz catheter [33, 34, 39]. According to Ranucci [44], first degree of diastolic dysfunction of the left ventricle is depicted as impaired relaxation, is usually observed just after discontinuation of cardiopulmonary bypass, and is often reversible (temporary). Second degree mimicking pseudo-normalization, is a more severe condition, which sometimes is an intermediate step towards, third degree of dysfunction which is characterized by a restrictive pattern. An increased ratio (> 2) between E and A waves of transmitral flow, and a blunted systolic waveform of the pulmonary vein flow is present due to left atrial pressure [34, 36, 39]. It has been demonstrated that mitral and pulmonary vein flow indexes correlate with pulmonary capillary wedge pressure (PCWP) [44, 45]. Therefore, additional measurement of PCWP by using a Swan-Ganz catheter may be in this phase useful in estimating the time course of diastolic dysfunction and the effect of therapeutic manipulations [44]. Fluid responsiveness is better defined by TOE derived variables (left ventricular end-diastolic area, peak blood velocity variation), but some information can be derived by the Swan-Ganz catheter as well (PCWP and peak pulmonary pressure variation) [45, 46]. In table 2 we present the high risk groups for developing DD, while in table 3, we report articles looking into: the impact of diastolic dysfunction (DD) on patient's outcome following Cardiac Surgery.

Table 2 High risk groups for developing DD
Full size table
Table 3 Articles looking into: The impact of diastolic dysfunction (DD) on patient's outcome following Cardiac Surgery.
Full size table

Progression of DD following Cardiac surgery

Following coronary artery bypass grafting, DD is temporarily deteriorated (expressed as a decrease in E-max and an increase in A-max of transmitral flow) [47]. This deterioration of DD seems to persist, at least for the first three postoperative hours after coronary artery bypass grafting [48, 49]. In a similar way, Yamamoto et al by using classical ECHO after coronary artery bypass grafting, showed that DD was characterized by a decrease in E wave velocity, prolongation of the E wave DT, and a decrease of E/A ratio [43]. Potential implicated mechanisms are those of free oxygen radicals, altered intracellular calcium homeostasis, or both [50, 51]. Temporary improvement has been shown, especially if calcium channels blocking factors like diltiazem were perioperatively administered or added in the cardioplegic solution [43, 50, 52, 53]. For patients who underwent off-pump coronary artery bypass grafting (OPCAB), comparative studies on the postoperative changes in left ventricular diastolic function, have shown that, while left ventricular diastolic dysfunction impairment was observed in both groups (conventional CABG and OPCAB), it was more significantly impaired in the CABG group [54]. Other studies showed that right ventricular diastolic dysfunction was in a similar way significantly impaired after CABG and OPCAB [43, 55, 56], and this deterioration persisted in up to one year postoperatively [15]. In contrast to this, Shi et al who evaluated short- and long-term evolution of biventricular diastolic performance postoperatively in 49 pts who underwent coronary artery bypass grafting showed that postoperative deterioration of diastolic dysfunction had an absolute return to preoperative status at six months postoperatively [9].

Management of DD

According to a multivariate analysis by Bernard et al [13], left ventricular diastolic dysfunction was a better predictor of hemodynamic instability after cardiac surgery compared to systolic dysfunction. Treatment of the underlying disease is currently the most important therapeutic approach. In patients with tachycardia, use of b-blockers or calcium antagonists, is beneficial so as to prolong diastolic (filling) time [24, 57]. Treatment of atrial fibrillation by cardioversion or amiodarone infusion is indicated in patients with diastolic dysfunction [22, 24, 57]. In addition, digitalis may decelerate ventricular rate in cases of permanent atrial fibrillation, and contribute to better ventricular filling [58]. Denault et al [59] developed a diagnostic algorithm which they then applied to a group of 74 cardiac surgical patients, to determine whether moderate to severe left ventricular diastolic dysfunction (LVDD) and right ventricular diastolic dysfunction (RVDD) can predict difficult discontinuation of cardiopulmonary bypass. Patients with moderate to severe LVDD tended to have higher PCWP compared to those with normal to mild LVDD. The presence of moderate to severe RVDD was also associated with lower mean pulmonary artery pressure and lower cardiac index compared to patients with normal to mild RVDD. Difficult separation from cardiopulmonary bypass was present in 65.5% and 72% of patients with moderate/severe LVDD and RVDD respectively, in contrast to 40.9% and 48% of patients with normal/mild LVDD/RVDD. They concluded that moderate and severe degree of LVDD and RVDD can be identified with very good reproducibility, and both degrees of diastolic dysfunction are associated to difficult discontinuation from cardiopulmonary bypass [59]. During this effort, transesophageal echo is a needful tool to estimate the degree of diastolic dysfunction, as well as preload and afterload. Appropriate increase of volume load is a milestone of timing in order to discontinue cardiopulmonary bypass. Phosphodiesterase inhibitors seem to be beneficial for diastolic dysfunction improvement, and should be used in perioperatively [60]. In a similar way, Levosimendan may used in perioperative management of diastolic dysfunction [61]. It increases cardiac output and decreases pulmonary capillary wedge pressures. This mode of enhanced contractile force generation is achieved without an increase in myocardial oxygen consumption, intracellular calcium concentrations, or an adverse effect on diastolic function [61]. For the next postoperative days milestone of treatment remain diuretics, in doses which prevent dyspnea and liver congestion on one side, but not reduce the cardiac output on the other [57]. ACE inhibitors in combination with spironolactone are beneficial because they prevent excessive activation of rennin-angiotensin-aldosterone system, and improve ventricular relaxation although not yet confirmed [62, 63]. In contrast to systolic dysfunction, use of calcium antagonists alone or in combination with ACE, contributes effectively in hypertension control and has a beneficial influence on hypertrophic myocardium [23, 24, 58]. In patients with diastolic dysfunction due to hypertrophic cardiomyopathy (either idiopathic or due to acquired aortic valve stenosis), the main problem is to load the left ventricle with adequate volume (preload) because it is common to notice an echo-finding of low preload (i.e. very low left ventricular end-diastolic area), while the measured PCWP is found high [55]. Such patients need increased volumes, but each fluid administration should be carefully guided by constant measurement of PCWP, in order to avoid an abrupt increase in pulmonary venous pressure and consequent acute pulmonary oedema [55]. Postoperatively, use of intra-aortic balloon pump in patients with left ventricular diastolic dysfunction seems to result in a favourable influence on left ventricular function [34]. Possible explanations for this effect lie on the positive effects of balloon on coronary flow against ischemia, the favourable effect on systolic function of left ventricle, and the increase of left ventricular long axis [34]. For those cases whereby "restricted pattern" is diagnosed, inotropic agents should be considered. Maslow et al showed that the use of inotropes in 44 patients, who underwent AVR for stenosis, was associated with significantly larger increase in right ventricular ejection fraction and cardiac output after CPB [64]. Changes in cardiac output and index were more strongly correlated with changes in RVEF than LVEF. Lastly, infusion of a new B-natriuretic peptide (BNP) nesiritide was associated with increased CO in patients with diastolic dysfunction and low CO syndromes undergoing cardiac surgery, when other measures failed. This agent seems to offer an additional option to inotropes and fluid challenges perioperatively [65]. Castellá et al in an experimental study conducted in pigs in 2006, demonstrated that temporary LAD ischemia alters the normal sequential pattern of contraction responsible for ejection and suction through reduction of the systolic contractile force, and prolongation of the endocardial contraction into early diastole to disrupt the normal endocardial-epicardial sequence responsible for ventricular suction [66]. The systolic and diastolic effects of myocardial stunning were studied to evaluate the role of the endocardial and epicardial segments and to determine if preconditioning by Na+-H+ exchange (NHE) inhibition effect post-stunning dysfunction. In this study conducted in Yorkshire-Duroc pigs, NHE inhibition before ischemia limits postischemic systolic and diastolic dysfunction by re-establishing the expected shortening sequences within the ventricular myocardial band model [66].

Conclusion

There are only few studies looking in to the impact of DD on the outcome following cardiac surgery. Without doubt DD with elevated left ventricular end-diastolic pressure can predispose to increased perioperative mortality and morbidity. Furthermore, DD is often associated with systolic dysfunction, left ventricular hypertrophy or indeed pulmonary hypertension. The mainstay of management of DD starts with the prompt recognition and diagnosis of this entity and relies on the aggressive management of the underlie aetiology of this insidious disease.

References

  1. Kitzman DW, Little WC, Brubaker PH, Anderson RT, Hundley WG, Marburger CT, Brosnihan B, Morgan TM, Stewart KP.: Pathophysiological characterization of isolated diastolic heart failure in comparison to systolic heart failure. JAMA. 2002, 288: 2144-50. 10.1001/jama.288.17.2144.

    Article  PubMed  Google Scholar 

  2. Rodeheffer R, Miller W, Burnett J: Pathophysiology of circulatory failure. Mayo Clinic Practice of Clinical Cardiology. Edited by: Giuliani E, Gersh B, Megoon M, Hayes D, Schaff H. 1996, Mosby, 556-58. 3

    Google Scholar 

  3. Vasan R, Benjamin E, Levy D: Prevalence, clinical features and prognosis of diastolic heart failure: an epidemiologic perspective. J Am Coll Cardiol. 1995, 26: 1565-74. 10.1016/0735-1097(95)00381-9.

    Article  CAS  PubMed  Google Scholar 

  4. Kramer K, Kirkman P, Kitzman D, Little WC.: Flash pulmonary edema: association with hypertension and reoccurrence despite coronary revascularization. Am Heart J. 2000, 140: 451-5. 10.1067/mhj.2000.108828.

    Article  CAS  PubMed  Google Scholar 

  5. Givetz M, Colucci W, Braunwald E: Clinical aspects of heart failure;Pulmonary edema, High-output failure. Braunwald's Heart Disease. Edited by: Zipes D, Libby P, Bonnow R, Braunwald E. 2005, Elsevier Saunders, 541-43. 7

    Google Scholar 

  6. Lappas DG, Skubas NJ, Lappas GD, Ruocco E, Tambassis E, Pasque M.: Prevalence of left ventricular diastolic filling abnormalities in adult cardiac surgical patients: an intraoperative echocardiographic study. Sem Thorac Cardiovasc Surg. 1999, 11: 125-33.

    Article  CAS  Google Scholar 

  7. Djaiani GN, McCreath BJ, Ti LK, Mackensen BG, Podgoreanu M, Phillips-Bute B, Mathew JP.: Mitral flow propagation velocity identifies patients with abnormal diastolic function during coronary artery bypass graft surgery. Anesth Analg. 2002, 95: 524-30. 10.1097/00000539-200209000-00004.

    PubMed  Google Scholar 

  8. Mathison M, Edgerton JR, Horswell JL, Akin JJ, Mack MJ.: Analysis of hemodynamic changes during beating heart surgical procedures. Ann Thorac Surg. 2000, 70: 1355-61. 10.1016/S0003-4975(00)01590-3.

    Article  CAS  PubMed  Google Scholar 

  9. Shi Y, Denault AY, Couture P, Butnaru A, Carrier M, Tardif JC: Biventricular diastolic filling patterns after coronary artery bypass graft surgery. J Thorac Cardiovasc Surg. 2006, 131: 1080-86. 10.1016/j.jtcvs.2006.01.015.

    Article  PubMed  Google Scholar 

  10. Malouf JF, Enriquez-Sarano M, Pellikka PA, Oh JK, Bailey KR, Chandrasekaran K, Mullany CJ, Tajik AJ.: Severe pulmonary hypertension in patients with severe aortic stenosis: clinical profile and prognostic implications. JACC. 2002, 40: 789-95.

    Article  PubMed  Google Scholar 

  11. Royse CF, Royse AG, Blake DW, Grigg LE.: Instantaneous end diastolic stiffness (IEDS): a simple, load independent measurement of left ventricular diastolic function in patients undergoing cardiacsurgery. Ann Thorac Cardiovasc Surg. 2000, 6: 203-10.

    CAS  PubMed  Google Scholar 

  12. Kim Y-J, Sohn D-W: Mitral annulus velocity in the estimation of left ventricular filling pressure; prospective study in 200 patients. J Am Soc Echocardiogr. 2000, 13: 980-5. 10.1067/mje.2000.107156.

    Article  CAS  PubMed  Google Scholar 

  13. Bernard F, Denault A, Babin D, Goyer C, Couture P, Couturier A, Buithieu J.: Diastolic dysfunction is predictive of difficult weaning from cardiopulmonarybypass. Anesth Analg. 2001, 92: 291-98. 10.1097/00000539-200102000-00002.

    Article  CAS  PubMed  Google Scholar 

  14. Lappas DG, Skubas NJ, Lappas GD, Ruocco E, Tambassis E, Pasque M: Prevalence of left ventricular diastolic filling abnormalities in adult cardiac surgical patients: an intraoperative echocardiographicstudy. Sem Thorac Cardiovasc Surg. 1999, 11: 125-33.

    Article  CAS  Google Scholar 

  15. Alam M, Hedman A, Nordlander R, Samad B.: Right ventricular function before and after an uncomplicated coronary artery bypass graft as assessed by pulsed wave Doppler tissue imaging of the tricuspid annulus. Am Heart J. 2003, 146: 520-26. 10.1016/S0002-8703(03)00313-2.

    Article  PubMed  Google Scholar 

  16. Grossman W: Defining diastolic dysfunction. Circulation. 2000, 101: 2020-1.

    Article  CAS  PubMed  Google Scholar 

  17. Liu J, Tanaka N, Murata K, Ueda K, Wada Y, Oyama R, Matsuzaki M.: Prognostic value of pseudonormal and restrictive filling patterns on left ventricular remodeling and cardiac events after coronary artery bypass grafting. Am J Cardiol. 2003, 91: 550-54. 10.1016/S0002-9149(02)03304-0.

    Article  PubMed  Google Scholar 

  18. Vaskelyte J, Stoskute N, Kinduris S, Ereminiene E.: Coronary artery bypass grafting in patients with severe left ventricular dysfunction: predictive significance of left ventricular diastolic filling pattern. Eur J Echocardiogr. 2001, 2: 62-67.

    Article  CAS  PubMed  Google Scholar 

  19. Natsuaki M, Itoh T, Ohteki H, Minato N, Ishii K, Suda H.: Evaluation of left ventricular early diastolic function after coronary artery bypass grafting relating to myocardial damage. Jpn Circ J. 1991, 55: 117-24.

    Article  CAS  PubMed  Google Scholar 

  20. Houltz E, Hellström A, Ricksten SE, Wikh R, Caidahl K: Early effects of Coronary artery bypass surgery and cold cardioplegic ischemia on left ventricular diastolic function: evaluation by computerassisted transesophageal echocardiography. J Cardiothorac Vasc Anesth. 1996, 10: 728-33. 10.1016/S1053-0770(96)80197-2.

    Article  CAS  PubMed  Google Scholar 

  21. Hogg K, Swedberg K, McMurray J: Heart failure with preserved left ventricular systolic function: Epidemiology, clinical characteristics, and prognosis. JACC. 2004, 43: 317-327.

    Article  PubMed  Google Scholar 

  22. Zile M, Brutsaerd D: New concepts in diastolic dysfunction and diastolic heart failure: Part I: Diagnosis, prognosis, and measurement of diastolic function. Circulation. 2002, 105: 1387-93. 10.1161/hc1102.105289.

    Article  PubMed  Google Scholar 

  23. Zile M, Brutsaerd D: New concepts in diastolic dysfunction and diastolic heart failure: Part II: Causal mechanisms and treatment. Circulation. 2002, 105: 1503-8. 10.1161/hc1202.105290.

    Article  PubMed  Google Scholar 

  24. Angeja B, Grossman W: Evaluation and management of diastolic heart failure. Circulation. 2003, 11; 107 (5): 659-63. 10.1161/01.CIR.0000053948.10914.49.

    Article  Google Scholar 

  25. Naqvi T: Diastolic function assessment incorporating new techniques in Doppler echocardiography. Rev Cardiovasc Med. 2003, 4: 81-99.

    PubMed  Google Scholar 

  26. Braunwald E, Zipes DP, Libby P: Normal and abnormal cardiac function: mechanisms of cardiac contraction and relaxation. Heart Diseases. Edited by: Zohrab R, GeryL, Reilly S etal. 2001, Philadelphia: WB Saunders Company, 451-4. 6

    Google Scholar 

  27. Cain BS, Meldrum DR, Joo KS, Wang JF, Meng X, Cleveland JC, Banerjee A, Harken AH.: Human SERCA2a levels correlate inversely with age in senescent human myocardium. JAAC. 1998, 32: 458-67.

    CAS  Google Scholar 

  28. Lubien E, DeMaria A, Krishnaswamy P, Clopton P, Koon J, Kazanegra R, Gardetto N, Wanner E, Maisel AS.: Utility of B-natriuretic peptide in detecting diastolic dysfunction: comparison with Doppler velocity recordings. Circulation. 2002, 105: 595-601. 10.1161/hc0502.103010.

    Article  CAS  PubMed  Google Scholar 

  29. European Study Group on Diastolic Heart Failure. How to diagnose diastolic heart failure. Eur Heart J. 1998, 19: 990-1003. 10.1053/euhj.1998.1057.

  30. Zile M, Baicu C, Gaasch W: Diastolic heart failure-Abnormalities in active relaxation and passive stiffness of the left ventricle. N Engl J Med. 2004, 350: 1953-59. 10.1056/NEJMoa032566.

    Article  CAS  PubMed  Google Scholar 

  31. McKenney PA, Apstein CS, Mendes LA, Connelly GP, Aldea GS, Shemin RJ, Davidoff R.: Increased left ventricular diastolic chambers stiffness immediately after coronary artery bypass surgery. JAAC. 1994, 24: 1189-94.

    CAS  Google Scholar 

  32. Nishimura R, Tajik A: Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician's Rosetta stone. JAAC. 1997, 30: 8-18.

    CAS  Google Scholar 

  33. Yamamoto K, Masuyama T, Tanouchi J, Doi Y, Kondo H, Hori M, Kitabatake A, Kamada T.: Effects of heart rate on left ventricular filling dynamics: Assessment from simultaneous recordings of pulsed Doppler transmitral flow velocity pattern and hemodynamic variables. Cardiovasc Res. 1993, 27: 935-41. 10.1093/cvr/27.6.935.

    Article  CAS  PubMed  Google Scholar 

  34. Maaten van der JM, de Vries AJ, Henning RH, Epema AH, Berg van den MP, Lip H: Effects of preoperative treatment with diltiazem on diastolic ventricular function after coronary artery bypass graft surgery. J CardiothoracVasc Anesth. 2001, 15: 710-16. 10.1053/jcan.2001.28314.

    Article  Google Scholar 

  35. Kessler KM: Diastolic heart failure. Diagnosis andmanagement. Hosp Pract (Off Ed). 1989, 24 (7): 137-41.

    Article  CAS  Google Scholar 

  36. Tresch D, McGough M: Heart failure with normal systolic function: a common disorder in old people. J Am Geriatr Soc. 1995, 43: 1035-42.

    Article  CAS  PubMed  Google Scholar 

  37. Ridker PM, Rifai N, Rose L, Buring JE, Cook NR: Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002, 347: 1557-65. 10.1056/NEJMoa021993.

    Article  CAS  PubMed  Google Scholar 

  38. De Boeck BW, Cramer MJ, Oh JK, Aa van der RP, Jaarsma W: Spectral pulsed tissue Doppler imaging in diastole: a tool to increase our insight in and assessment of diastolic relaxation of the leftventricle. Am Heart J. 2003, 146: 411-9. 10.1016/S0002-8703(03)00322-3.

    Article  PubMed  Google Scholar 

  39. Nagueh SF, Lakkis NM, Middleton KJ, Spencer WH, Zoghbi WA, Quiñones MA.: Doppler estimation of left ventricular filling pressures in patients with hypertrophic cardiomyopathy. Circulation. 1999, 99: 254-61.

    Article  CAS  PubMed  Google Scholar 

  40. Bonow R, Udelson J: Left ventricular diastolic dysfunction as a cause of congestive heart failure: mechanisms and mangament. AnnIntern Med. 1992, 117: 501-10.

    Google Scholar 

  41. del Monte F, Williams E, Lebeche D, Schmidt U, Rosenzweig A, Gwathmey JK, Lewandowski ED, Hajjar RJ.: Improvement in survival and cardiac metabolism after gene transfer of sarcoplasmic reticulum Ca(2+)-ATPase in a rat model of heart failure. Circulation. 2001, 104: 1424-9. 10.1161/hc3601.095574.

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  42. De Hert SG, Linden Vander PJ, ten Broecke PW, De Mulder PA, Rodrigus IE, Adriaensen HF: Assessment of length-dependent regulation of myocardial function in coronary surgery patients using transmitral flow velocity patterns. Anesthesiology. 2000, 93: 374-81. 10.1097/00000542-200008000-00015.

    Article  CAS  PubMed  Google Scholar 

  43. Yamamoto K, Nishimura RA, Chaliki HP, Appleton CP, Holmes DR, Redfield MM: Determination of left ventricular filling pressure by Doppler echocardiography in patients with coronary artery disease: Critical role of left ventricular systolic function. JACC. 1997, 30: 1819-26.

    Article  CAS  PubMed  Google Scholar 

  44. Ranucci M: Which cardiac surgical patients can benefit from placement of a pulmonary artery catheter?. Crit Care. 2006, 10 (Suppl 3): S6-10.1186/cc4833.

    Article  PubMed  PubMed Central  Google Scholar 

  45. Lattik R, Couture P, Denault AY, Carrier M, Harel F, Taillefer J, Tardif JC.: Mitral doppler indices are superior to two-dimensional echocardiographic and hemodynamic variables in predicting responsiveness of cardiac output to a rapid intravenous infusion of colloid. Anesth Analg. 2002, 94: 1092-1099. 10.1097/00000539-200205000-00007.

    Article  PubMed  Google Scholar 

  46. DiCorte CJ, Latham P, Greilich PE, Cooley MV, Grayburn PA, Jessen ME.: Esophageal doppler monitor determinations of cardiac output and preload during cardiac operations. Ann Thorac Surg. 2000, 69: 1782-1786. 10.1016/S0003-4975(00)01129-2.

    Article  CAS  PubMed  Google Scholar 

  47. McKenney PA, Apstein CS, Mendes LA, Connelly GP, Aldea GS, Shemin RJ, Davidoff R.: Increased left ventricular diastolic chambers stiffness immediately after coronary artery bypass surgery. JAAC. 1994, 24: 1189-94.

    CAS  Google Scholar 

  48. Ekery DL, Davidoff R, Orlandi QG, Apstein CS, Hesselvik JF, Shemin RJ, Shapira OM.: Imaging and diagnostic testing: diastolic dysfunction after coronary artery bypass grafting: a frequent finding of clinical significance not influenced by intravenous calcium. Am Heart J. 2003, 145: 896-902. 10.1016/S0002-8703(02)94786-1.

    Article  PubMed  Google Scholar 

  49. Skarvan K, Filipovic M, Wang J, Brett W, Seeberger M.: Use of myocardial tissue Doppler imaging for intraoperative monitoring of left ventricular function. Br J Anesth. 2003, 91: 473-80. 10.1093/bja/aeg210.

    Article  CAS  Google Scholar 

  50. Gardin JM, Arnold AM, Bild DE, Smith VE, Lima JA, Klopfenstein HS, Kitzman DW: Left ventricular diastolic filling in the elderly: the cardiovascular health study. Am J Cardiol. 1998, 82: 345-51. 10.1016/S0002-9149(98)00339-7.

    Article  CAS  PubMed  Google Scholar 

  51. Hess M: Free radicals, calcium homeostasis, heat shock proteins, and myocardial stunning. Ann Thorac Surg. 1995, 60: 760-66. 10.1016/0003-4975(95)00574-5.

    Article  CAS  PubMed  Google Scholar 

  52. Malhotra R, Mishra M, Kler TS, Kohli VM, Mehta Y, Trehan N.: Cardioprotective effects of diltiazem infusion in the perioperativeperiod. Eur J Cardiothorac Surg. 1997, 12: 420-27. 10.1016/S1010-7940(97)00140-1.

    Article  CAS  PubMed  Google Scholar 

  53. Seitelberger R, Hannes W, Gleichauf M, Keilich M, Christoph M, Fasol R.: Effects of diltiazem on perioperative ischemia, arrhythmias, and myocardial function in patients undergoing elective coronary bypass grafting. J Thorac Cardiovasc Surg. 1994, 107: 811-21.

    CAS  PubMed  Google Scholar 

  54. Ng KK, Popovic ZB, Troughton RW, Navia J, Thomas JD, Garcia MJ.: Comparison of left ventricular diastolic function after on-pump versus off-pump coronary artery bypass grafting. Am J Cardiol. 2005, 95: 647-50. 10.1016/j.amjcard.2004.10.043.

    Article  PubMed  Google Scholar 

  55. Michaux I, Filipovic M, Skarvan K, Schneiter S, Schumann R, Zerkowski HR, Bernet F, Seeberger MD: Effects of on-pump versus off-pump coronary artery bypass graft surgery on right ventricularfunction. J Thorac Cardiovasc Surg. 2006, 131: 1281-88. 10.1016/j.jtcvs.2006.01.035.

    Article  PubMed  Google Scholar 

  56. Kwak YL, Oh YJ, Jung SM, Yoo KJ, Lee JH, Hong YW: Change in right ventricular function during off-pump coronary artery bypass graft surgery. Eur J Cardiothorac Surg. 2004, 25: 572-77. 10.1016/j.ejcts.2004.01.005.

    Article  CAS  PubMed  Google Scholar 

  57. Bristow M, Lowes B: Management of heart failure. Braunwald's Heart Disease. Edited by: Zipes D, Libby P, Bonnow R, Braunwald E. 2005, Elsevier Saunders, 610-7

    Google Scholar 

  58. Lee T: Management of heart failure. Braunwald's Heart Disease. Edited by: Zipes D, Libby P, Bonnow R, Braunwald E. 2005, Elsevier Saunders, 623-24. 7

    Google Scholar 

  59. Denault AY, Couture P, Buithieu J, Haddad F, Carrier M, Babin D, Levesque S, Tardif JC.: Left and right ventricular diastolic dysfunction as a predictors of difficult separation from cardiopulmonary bypass. Can J Anesth. 2006, 53: 1020-29. 10.1007/BF03022532.

    Article  PubMed  Google Scholar 

  60. Mitrovic V, Strasser R, Berwing K, Thormann J, Schlepper M.: Acute effects of enoximone after intracoronary administration on hemodynamics, myocardial perfusion, and regional wall motion. Z Kardiol. 1996, 85: 856-67.

    CAS  PubMed  Google Scholar 

  61. Ng T, Akhter M: Levosimendan: dual mechanisms for acute heart failure...and beyond?. Minerva Cardioangiol. 2005, 53: 565-84.

    CAS  PubMed  Google Scholar 

  62. Yusuf S, Pfeffer MA, Swedberg K, Granger CB, Held P, McMurray JJ, Michelson EL, Olofsson B, Ostergren J, CHARM Investigators and Committees: Effects of candesartan in patients with chronic heart failure and preserved left ventricular ejection fraction. Lancet. 1994, 362: 767-71.

    Google Scholar 

  63. Okura Y, Nakashima Y, Tojo H, Tashiro E, Saku K.: Valsartan, an angiotensin II typa-I receptor blocker, and left ventricular diastolic function. A case report. Angiology. 2005, 56: 67-73. 10.1177/000331970505600415.

    Article  Google Scholar 

  64. Maslow AD, Regan MM, Schwartz C, Bert A, Singh A.: Inotropes improve right heart function in patients undergoing aortic valve replacement for aortic stenosis. Anesth Analg. 2004, 98: 891-902. 10.1213/01.ANE.0000107940.23783.33.

    Article  PubMed  Google Scholar 

  65. Gordon GR, Schumann R, Rastegar H, Khabbaz K, England MR.: Nesiritide for treatment of perioperative low cardiac output syndromes in cardiac surgical patients: an initial experience. J Anesth. 2006, 20: 307-11. 10.1007/s00540-006-0430-9.

    Article  PubMed  Google Scholar 

  66. Castellá M, Buckberg GD, Saleh S: Diastolic dysfunction in stunned myocardium: a state of abnormal excitation-contraction coupling that is limited by Na+-H+ exchange inhibition. Eur J CardiothoracSurg. 2006, 29 (Suppl 1): S107-14. 10.1016/j.ejcts.2006.02.042. Epub 2006 Mar 27.

    Article  Google Scholar 

  67. Paulus WJ, Shah AM: NO and cardiac diastolic function. Cardiovasc Res. 1999, 43 (3): 595-606. 10.1016/S0008-6363(99)00151-0.

    Article  CAS  PubMed  Google Scholar 

  68. Bruch C, Schmermund A, Marin D, Katz M, Bartel T, Schaar J, Erbel R: Tei-index in patients with mild-to-moderate congestiveheart failure. Eur Heart J. 2000, 21 (22): 1888-95. 10.1053/euhj.2000.2246.

    Article  CAS  PubMed  Google Scholar 

  69. Mandinov L, Eberli FR, Seiler C, Hess OM: Diastolic heartfailure. Cardiovasc Res. 2000, 45 (4): 813-25. 10.1016/S0008-6363(99)00399-5.

    Article  CAS  PubMed  Google Scholar 

  70. Vasan RS, Levy D: Defining diastolic heart failure: a call for standardized diagnostic criteria. Circulation. 2000, 102: 2118-2121.

    Article  Google Scholar 

  71. Zile MR, Gaasch WH, Carroll JD, Feldman MD, Aurigemma GP, Schaer GL, Ghali JK, Liebson PR: Heart failure with a normal ejection fraction: is measurement of diastolic function necessary to make the diagnosis of diastolic heart failure?. Circulation. 2001, 104 (7): 779-82. 10.1161/hc3201.094226.

    Article  CAS  PubMed  Google Scholar 

  72. Poulsen SH: Clinical aspects of left ventricular diastolic function assessed by Doppler echocardiography following acute myocardial infarction. Dan Med Bull. 2001, 48 (4): 199-210.

    CAS  PubMed  Google Scholar 

  73. Catuzzo B, Ciancamerla F, Bobbio M, Longo M, Trevi GP: In patients with severe systolic dysfunction, only brain natriuretic peptide is related to diastolic restrictive pattern. J Card Fail. 2003, 9 (4): 303-10. 10.1054/jcaf.2003.44.

    Article  CAS  PubMed  Google Scholar 

  74. Yturralde RF, Gaasch WH: Diagnostic criteria for diastolic heart failure. Prog Cardiovasc Dis. 2005, 47 (5): 314-9. 10.1016/j.pcad.2005.02.007.

    Article  PubMed  Google Scholar 

  75. Zile MR, Baicu CF, Bonnema DD: Diastolic heart failure. Definitions and terminology. Prog Cardiovasc Dis. 2005, 47 (5): 307-13. 10.1016/j.pcad.2005.02.006.

    Article  PubMed  Google Scholar 

  76. Shammas RL, Khan NU, Nekkanti R, Movahed A: Diastolic heart failure and left ventricular diastolic dysfunction: what we know, and what we don't know!. Int J Cardiol. 2007, 115 (3): 284-92. 10.1016/j.ijcard.2006.03.027. Epub 2006 Aug 14.

    Article  PubMed  Google Scholar 

  77. Scardovi AB, Coletta C, Aspromonte N, Perna S, Greggi M, D'Errigo P, Sestili A, Ceci V: Brain natriuretic peptide plasma level is a reliable indicator of advanced diastolic dysfunction in patients with chronic heart failure. Eur J Echocardiogr. 2007, 8 (1): 30-6. 10.1016/j.euje.2005.12.009.

    Article  PubMed  Google Scholar 

  78. Sanderson J: Diastolic heart failure or heart failure with a normal ejection fraction. Minerva Cardioangiol. 2006, 54: 715-24.

    CAS  PubMed  Google Scholar 

  79. Aronson S, Boisvert D, Lapp W: Isolated systolic hypertension is associated with adverse outcomes from coronary artery bypass grafting surgery. Anesth Analg. 2002, 94: 1079-84. 10.1097/00000539-200205000-00005.

    Article  PubMed  Google Scholar 

  80. Rajan S, Gokhale S: Cardiovascular function in patients with insulin-dependent diabetes mellitus: a study using noninvasivemethods. Ann N Y Acad Sci. 2002, 958: 425-30.

    Article  CAS  PubMed  Google Scholar 

  81. Zola B, Kahn J, Juni J: Abnormal cardiac function in diabetic patients with autonomic neuropathy in the absence of ischemic heart disease. J Clin Endocrinol Metab. 1986, 63: 208-14. 10.1210/jcem-63-1-208.

    Article  CAS  PubMed  Google Scholar 

  82. Ewing D, Campbell I, Clarke B: Heart rate changes in diabetes mellitus. Lancet. 1981, 1: 183-6. 10.1016/S0140-6736(81)90061-1.

    Article  CAS  PubMed  Google Scholar 

  83. Yamada H, Goh PP, Sun JP, Odabashian J, Garcia MJ, Thomas JD, Klein AL: Prevalence of left ventricular diastolic dysfunction by Doppler echocardiography: clinical application of the Canadian Consensus Guidelines. J Am Soc Echocardiogr. 2002, 15: 1238-44. 10.1067/mje.2002.124877.

    Article  PubMed  Google Scholar 

  84. Casthely PA, Shah C, Mekhjian H, Swistel D, Yoganathan T, Komer C, Miguelino RA, Rosales R: Left ventricular diastolic function after coronary artery bypass grafting: a correlative study with three different myocardial protection techniques. J Thorac CardiovascSurg. 1997, 114 (2): 254-60. 10.1016/S0022-5223(97)70153-3.

    Article  CAS  Google Scholar 

  85. Malouf PJ, Madani M, Gurudevan S, Waltman TJ, Raisinghani AB, DeMaria AN, Blanchard DG: Assessment of diastolic function with Doppler tissue imaging after cardiac surgery: effect of the "postoperative septum" in on-pump and off-pump procedures. J Am Soc Echocardiogr. 2006, 19 (4): 464-7. 10.1016/j.echo.2005.12.001.

    Article  PubMed  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Cardiothoracic Surgery Department, School of Medicine, University of Patras, Patras, Greece

    Efstratios E Apostolakis & Nikolaos G Baikoussis

  2. Cardiac Surgery Department, School of Medicine, University of Ioannina, Ioannina, Greece

    Nikolaos G Baikoussis & Stavros N Siminelakis

  3. Basildon & Thurrock University Hospital NHS FT, Basildon, Essex, UK

    Haralabos Parissis

  4. Department of Clinical Anesthesiology and Intensive Postoperative Care Unit, School of Medicine, University of Ioannina, Ioannina, Greece

    Georgios S Papadopoulos

Authors
  1. Efstratios E Apostolakis
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Nikolaos G Baikoussis
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Haralabos Parissis
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Stavros N Siminelakis
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Georgios S Papadopoulos
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Nikolaos G Baikoussis.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

All authors: 1. have made substantial contributions to conception and design, or acquisition of data, or analysis and interpretation of data; 2. have been involved in drafting the manuscript or revisiting it critically for important intellectual content; 3. have given final approval of the version to be published.

Authors’ original submitted files for images

Below are the links to the authors’ original submitted files for images.

Authors’ original file for figure 1

Rights and permissions

Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/2.0 ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Reprints and permissions

About this article

Cite this article

Apostolakis, E.E., Baikoussis, N.G., Parissis, H. et al. Left ventricular diastolic dysfunction of the cardiac surgery patient; a point of view for the cardiac surgeon and cardio-anesthesiologist. J Cardiothorac Surg 4, 67 (2009). https://0-doi-org.brum.beds.ac.uk/10.1186/1749-8090-4-67

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/1749-8090-4-67

Keywords

Journal of Cardiothoracic Surgery

ISSN: 1749-8090

Contact us