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Transcript
Diastolic Dysfunction and Anaesthetic Implications
Dr S Kumar MD PhD
Sr Consultanat & Head, Cardiac Anesthesiology,
Meenakshi Mission Hospital and Research Centre, Madurai.
Epidemiological and clinical studies have confirmed the trend of increasing incidence of chronic
HF internationally [1]. HF remains largely a disease of the elderly and in patients older than 65
years it is the most common diagnosis at hospital discharge and the most frequent cause of
readmission [2]. Diastolic dysfunction refers to abnormalities in left ventricular distensibility,
filling or relaxation regardless of signs and symptoms of HF or left ventricular ejection fraction .
Diastolic dysfunction in the absence of symptoms is common in elderly hypertensive patients.
Heart failure with a preserved ejection fraction (HFpreEF), or diastolic HF, refers to the clinical
syndrome of HF coupled with evidence of diastolic dysfunction and is estimated to occur in
approximately 50% of patients with chronic HF [3].
In patients older than 70 years, the adjusted mortality rate for HFpreEF is equivalent to those
patients with reduced systolic function [3]. It is projected that in the developed world the
proportion of the population >65 years old and the number of surgical procedures in this group of
patients will increase dramatically with at least one in two persons undergoing an operation in
the remainder of their lifetime . It is therefore imperative that anaesthetists and intensivists
appreciate the impact of diastolic dysfunction and HFpreEF on the aging heart.
DEFINITION
In 1998 Paulus et al. developed the European Criteria for HFpreEF [4]. This group suggested
that there must be objective evidence of HF with a normal or mildly impaired systolic function
(left ventricular ejection fraction (LVEF) > 45%) and abnormal left ventricular (LV) relaxation.
All three criteria are required for the diagnosis of HFpreEF. Plasma levels of B-natriuretic
peptide (BNP) are elevated in patients with HF, independent of the aetiology of HF [5]. The
updated consensus statement from the European Society of Cardiology is summarized in Table 1.
This report considers an LV wall index >122 g/m2 or an LV wall mass index >149 g/m2, in the
presence of symptoms, adequate evidence for the diagnosis of diastolic HF when other
modalities such as Tissue Doppler Imaging (TDI) are inconclusive in the context of elevated
BNP levels [6].
Table 1. The European Society of Cardiology Criteria for Diastolic Heart Failure[6]
The European consensus criteria for diastolic HF
1. Signs and symptoms of CHF
Effort dyspnoea, orthopnea, pulmonary rales/oedema.
Cardiopulmonary exercise testing (VO2max
< 25 ml/kg/min)
2. Normal or mildly reduced ejection fraction and
normal chamber size
LVEF > 50% and
Normal LV end diastolic volume(<97 mL/m2)
3. Abnormal LV relaxation, filling or diastolic
distensibility or stiffness
Echocardiographic: Tissue Doppler (E/Ea > 15)
LA volume P34 ml/m2 if E/Ea between 9 and 14
Cardiac catheterisation: LVEDP > 16 mmHg
Biomarkers NT-proBNP > 220 pg/ml or BNP > 200 pg/
Ml
All three criteria are required for the diagnosis of diastolic heart failure
PATHOPHYSIOLOGY
The four phases of diastolic function are depicted in Fig. 1. The structural, functional and
molecular mechanisms involved in diastolic dysfunction can conceptually be divided in those
that occur at the cardiomyocyte level and those that are extrinsic to the myocyte.
Figure 1. The four phases of diastole. The first point of intersection marks the end of the isovolumic relaxation (IR)
phase and mitral valve opening. In the rapid filling phase the left atrial (LA) pressure is higher than the left
ventricular (LV) pressure. The second pont of intersection LV pressure exceeds LA pressure resulting in
decelerating flow. During the slow filling phase there is almost no pressure difference between the two chambers.
Atrial contraction raises the LA pressure above the LV pressure. The period between the first two intersection points
corresponds to the E wave seen on transmitral flow.
CARDIOMYOCYTE
At the myocyte level, changes in calcium homeostasis result in an increased diastolic cytosolic
calcium. This may be as a result of (1) abnormalities in the sarcoplasmic reticulum calcium (SR
Ca2+) reuptake due to decreases in SR Ca2+ ATPase (2) abnormalities in the ionic channels
responsible for calcium transport, and (3) changes in the state of phosphorylation of proteins
such as phospholamban, calmodulin and calsequestrin that modify SR Ca2+ ATPase function .
Increased cytosolic calcium causes abnormalities in both active relaxation and passive stiffness.
Altered troponin I function, a shift towards higher intracellular Na+, Changes in the
cardiomyocyte cytoskeleton proteins and abnormalities in myocardial phosphate metabolism can
produce diastolic dysfunction [7].
EXTRACELLULAR MATRIX
The myocardial extracellular matrix is a dynamic tissue that responds to environmental cues and
tissue injury. Changes in fibrillar collagen may be responsible for the development of diastolic
dysfunction and diastolic HF [7]. Increased matrix metalloproteinases (MMP) activity results in
a 2-tiered response. Initially the myocytes respond to increased collagen destruction by
myocardial hypertrophy and increased collagen production. Over a period of time, there is a
decreased rate of pressure decrement during diastole [7]. Elevations of collagen turnover occur in
patients with asymptomatic diastolic dysfunction as well as diastolic HF [7]. In addition, the
magnitude of collagen turnover correlates directly with the severity of diastolic dysfunction[7].
AGE RELATED CHANGES IN DIASTOLIC FUNCTION
During aging, changes related to increased myocardial and ventricular stiffening and diminished
β-adrenergic receptor responsiveness are highly significant. At the myocyte level, age-related
reductions in SERCA2 levels and activity result in abnormal diastolic sequestration of calcium
[8]. An increase in activity of phospholamban also impairs diastolic function. Aging is associated
with a β-adrenergic associated signal dampening [9]. This may be due to receptor down
regulation or due to reduced receptor coupling to adenyl cyclase via Gs proteins. Age related
degeneration of the conducting system makes elderly patients prone to arrhythmia and further
compromises diastolic function . Aging is associated with systolic-ventricular and arterial
stiffening , which may influence diastolic function in several ways. Arterial stiffening increases
myocardial oxygen consumption for a given stroke volume and ventricular systolic stiffening
exacerbates this effect. The increased arterial stiffness results in ventricular hypertrophy to
preserve systolic function at the expense [10].
ASSESSMENT OF DIASTOLIC FUNCTION
ECHOCARDIOGRAPHY
In the perioperative and critical care context, Transthoracic echocardiography (TTE) is often
technically challenging. This may be due to difficulties with patient positioning, or a reduction of
the acoustic window by high levels of positive end expiratory pressure, the presence of injuries,
drains or dressings on the precordial area. Transesophageal echocardiography (TEE) has been
recommended to overcome these limitations . The reference ranges are derived from awake
patients undergoing TTE in the lateral decubitus position. This is in contrast to the supine
anaethetised patient receiving mechanical ventilation under dynamic haemodynamic conditions
influenced by anaesthetic drugs. A summary of the criteria commonly used to define diastolic
dysfunction is presented in Table 2.Refinements in echocardiography technology include Tissue
Doppler Imaging (TDI), colour TDI, strain and strain rate and have become an important part of
clinical practice. TDI has two important limitations. Firstly, the measured velocities are
dependent on the angle of insonation. Secondly TDI is of limited utility in analyzing regional
wall motion abnormalities as TDI cannot differentiate actively contracting myocardium from
infarcted myocardium that is tethering.
PROGNOSIS
Several variables have been identified as independent clinical predictors of mortality in patients
with HF. These include age, New York Heart Association Class IV symptoms, CAD, Diabetes,
peripheral vascular disease and the presence of valvular heart disease. Whether patients survive
longer after a diagnosis of systolic HF than a diagnosis of systolic HF is still debated [7].
Hospital readmission rates and length of hospital stay for patients with HFpreEF are similar to
SHF and the former have a higher likelihood of functional limitations or labile symptoms on
follow-up [7].
Table 2. Criteria used to define diastolic dysfunction (modified from Nageuh et al. [11] and
Gabriel et al. [12]
Criteria
Normal adult
E/A ratio
Deceleration
time (ms)
IVRT (ms)
1–2
150–240
Impaired
relaxation (stage 1)
Pseudonormal
(stage 2)
<1
1–1.5 (reverses with
Valsalva maneuver)
>240
150–200
Reversible
restrictive (stage 3)
Irreversible restrictive
(stage 4)
>1.5
1.5–2 (no change with
Valsalva maneuver)
<150
<150
<70
70–90
>90
<90
<70
PV S/D ratio
>1
>1
<1
<1
PV Arev-MV A
wave (ms)
<0
<0 or >30
>30
>30
>30
Arev velocity
(cm2)
<35
<35
>35
>35
>35
Vp
>55
E’ velocity
>8
LA volume
index
<34 ml/m2
>45
<1
<45
<45
<45
<8
<8
<8
<8
<34 ml/m2
>34 ml/m2
>34 ml/m2
>34 ml/m2
When outcome from HF is adjusted for the contribution of co-morbidity, there is a uniformly
poor prognosis regardless of the ejection fraction. Information regarding the prognosis in
asymptomatic diastolic dysfunction is sparse. A community based study of 2042 patients 45
years and older found that patients with diastolic dysfunction without a history of cardiac failure
have a significant risk of death [13].
ANAESTHETIC IMPLICATIONS
PRE-OPERATIVE ASSESSMENT
There is no specific risk model for predicting perioperative risk in patients with HfpreEF. When
planning surgical procedures in patients with stable HF, it is important to identify those patients
that are unlikely to survive long enough to accrue benefit from the procedure. Data from studies
describing the clinical profile of cardiac transplant patients have highlighted the difficulties in
predicting survival in patients with advanced HF. There is limited data on perioperative risk
stratification for isolated diastolic dysfunction. Patients requiring vascular surgery have been
shown to frequently have asymptomatic isolated diastolic dysfunction that is associated with a
significantly higher rate of major adverse cardiovascular events (MACE) [7]. Isolated diastolic
dysfunction has been shown to increase the risk for postoperative atrial fibrillation in cardiac
surgical patients [14]. These observations make a compelling case for the routine assessment of
perioperative diastolic function.
EXERCISE CAPACITY AND DIASTOLIC DYSFUNCTION
Exercise capacity is a useful pre-operative screening test. Exercise intolerance is often the
earliest clinical presentation of diastolic dysfunction and is a major determinant of quality of life.
During exercise, patients with diastolic dysfunction are unable to augment their cardiac output by
increasing their end diastolic volume. Left ventricular end diastolic pressure and pulmonary
venous pressure rises, reducing the pulmonary compliance and increasing the work of breathing.
IMPLICATIONS IN THE PERIOPERATIVE PERIOD
It is highly likely that elderly patients with vascular disease or hypertension would have some
degree of diastolic dysfunction [7]. Induction of anaesthesia results in significant alterations in
ventricular filling in patients with diastolic dysfunction. In patients requiring cardiac surgery,
diastolic dysfunction has been shown to be a better predictor of haemodynamic instability than
systolic dysfunction [15]. Moderate and severe diastolic dysfunction is also independently
associated with difficulties with separation from cardiopulmonary bypass [15]. Pre-operative
diastolic dysfunction is associated with a range of adverse outcomes including higher mortality,
worse mitral regurgitation and longer hospital stay in patients requiring surgical ventricular
restoration, mitral valve annuloplasty or elective vascular surgery. The presence of pre-operative
diastolic dysfunction is a strong independent predictor for developing post-operative atrial
fibrillation after cardiac surgery. There are two mechanism by which acute myocardial ischaemia
induces diastolic dysfunction [7] .The first mechanism is by arterial hypoxaemia and occurs
within 2 min, The second mechanism is by perfusion ischaemia and occurs at about 20–30 min.
Diastolic dysfunction is commonly associated with LVH.
The choice of anaesthetic technique has been shown to influence diastolic properties in patients
with preexisting diastolic dysfunctiona balanced anaesthetic technique with positive pressure
ventilation, no difference between sevoflurane and propofol on diastolic function was observed
[16]. The mechanism by which propofol affects diastolic function is similar to volatile
anaesthesia.
DIASTOLIC DYSFUNCTION AND SEPSIS
The occurrence of myocardial dysfunction in patients with sepsis carries a significant burden of
mortality (70%) compared with those patients that do not have myocardial dysfunction. Munt et
al., have demonstrated similar abnormalities in diastolic performance in a group of 24 critically
ill patients [17]. This report also identified abnormalities of LV filling as being independently
predictive of mortality. Baitugaeva et al. examined diastolic performance in 59 patients between
the ages of 18– 24 years with sepsis, severe sepsis and septic shock and noted a significant
relationship between diastolic dysfunction and pro-inflammatory cytokines [18].
PEDIATRIC PATIENTS WITH CARDIAC DISEASE
A study of cardiac growth in healthy children using TDI showed a correlation between diastolic
function and age [7]. ASD closure in adult patients is characterised by an increase in left
ventricular dimensions, elevations in N-terminal proBNP, delayed improvement in exercise
tolerance and even HF [19]. This makes a convincing case for early closure of ASD. Recent
studies using TDI and strain rate and strain, after complete repair of TOF, have found significant
systolic and diastolic dysfunction of the right ventricle. These patients have a significant risk of
late right ventricular failure, and pulmonary insufficiency [20]. These reports provide further
evidence that complete repair of TOF should be performed during infancy as delayed repair
exposes the myocardium to chronic hypoxaemia and hypertrophy.
TREATMENT
The treatment of diastolic heart failure is less well defined than the treatment of systolic heart
failure.
NONPHARMACOLOGIC INTERVENTIONS
Lifestyle modifications are recommended to reduce the risk of all forms of cardiovascular
disease. Measures include weight loss, smoking cessation, dietary changes, and exercise.
Identification and treatment of comorbid conditions, such as high blood pressure, diabetes, and
hypercholesterolemia, are important in reducing the risk of subsequent heart failure.[25]
PHARMACOLOGIC THERAPY
Pharmacologic treatment of diastolic heart failure is directed at normalizing blood pressure,
promoting regression of left ventricular hypertrophy, preventing tachycardia, treating symptoms
of congestion, and maintaining atrial contraction.[25] The basis for drug therapy remains
empiric, and the recommendations discussed in this section come from the ACC/AHA guidelines
and the ICSI evidence-based practice guideline.[25]
Treatment with diuretics and vasodilators often is necessary to reduce pulmonary congestion.
However, caution is required to avoid excessive diuresis, which can decrease preload and stroke
volume. Patients with diastolic dysfunction are highly sensitive to volume changes and preload.
The potential benefits of beta blockers stem from their ability to decrease heart rate, increase
diastolic filling time, decrease oxygen consumption, lower blood pressure, and cause regression
of left ventricular hypertrophy. The multiple benefits of angiotensin-converting enzyme (ACE)
inhibitors in the treatment of cardiovascular disease make them highly promising therapeutic
agents. ACE inhibitors cause regression of left ventricular hypertrophy, decrease blood pressure,
and prevent or modify cardiac remodeling; these actions provide strong theoretical support for
the use of these agents in patients with diastolic dysfunction.
In theory, the use of calcium channel blockers may be beneficial, because these agents decrease
blood pressure, decrease oxygen demand, and dilate coronary arteries. However, data are lacking
on patient-oriented outcomes such as morbidity and mortality. Calcium channel blockers should
be used with caution in patients with coexisting systolic and diastolic dysfunction. The longacting dihydropyridine class of calcium channel blockers is safe for use in patients with systolic
heart failure, but nondihydropyridine agents should be avoided.
CONCLUSION
Diastolic dysfunction and HF remain underappreciated in the peri-operative and critical care
environment. Epidemiological data predict that diastolic HF will become the more frequently
encountered type of HF encountered in clinical practice. Advances in echocardiography
technology have been instrumental in our understanding of ventricular function. Currently,
therapeutic options specific to this group of patients is limited and mortality has remained
unchanged. In contrast to patients with reduced EF, the prognosis for those with HTPreEF has
failed to improve in the last three decades. The potential public health burden should make
diastolic dysfunction and diastolic HF a priority.
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