STEMI Intervention – A Review of Relevant Clinical Trials.
Sameer Mehta, Raghotham R. Patlola, salomon Cohen,
Esther falcao, Ana Isabel Flores, estefania Oliveros Soles
Mercy Medical Center, Miami Florida, USA
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In last two decades there is a substantial increase in prevalence of Diastolic Heart failure (DHF) from 38 % to 54%1,2. The prognosis of patients suffering from DHF is as ominous as prognosis of patients suffering from Systolic Heart failure (SHF)3-8. The various predisposing factors are old age, female gender, metabolic syndrome, diabetes, arterial hypertension and left ventricular hypertrophy9-10. Elderly patients usually present with DHF in the setting of acute myocardial infarction11. As there is epidemiological evolution towards DHF in the population all over the world, a reappraisal of original established set of criteria is necessary for diagnosis of DHF. However, newer modalities of Echo-Doppler strain techniques may help in predicting the precursors of DHF. These echo variables include Left atrial (LA) strain & strain rate, LA stiffness and LA ejection fraction. Segmental left
PATHOPHYSIOLOGY
Diastole is the process by which the heart returns to its relaxed state; it is also the time for cardiac perfusion. Drastic
Email: drhkchopra@yahoo.com
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changes occur in cardiac pressure-volume relationships during
diastole. The diastolic process has four identifiable phases:
isovolumetric relaxation time, the time of aortic valve closure
to mitral valve opening; early rapid filling after mitral valve
opening; diastasis, a period of low flow during mid-diastole
and late filling of the ventricles by atrial contraction (Figure
1).
 |
| Figure.1. Cardiac cycle, showing changes in left atrial pressure, left ventricular pressure, aortic pressure, and ventricular volume; the electrocardiogram (ECG); and the phonocardiogram |
Diastole is a complex process that is affected by a number of
factors, including hypertension, ischemia, heart rate, velocity
of relaxation, cardiac compliance (i.e., elastic recoil and
stiffness), hypertrophy and segmental wall coordination of
the heart muscle. The pathophysiology of diastolic dysfunction includes delayed relaxation, impaired LV filling and/or increased stiffness. These conditions result typically in an upward displacement of the diastolic pressure–volume relationship with increased end-diastolic, left atrial and pulmocapillary wedge pressure leading to DHF. Chronic hypertension is the most common cause of diastolic dysfunction and failure. It leads to left ventricular hypertrophy and increased connective tissue content, both of which decrease cardiac compliance17. The hypertrophied ventricle has a steeper diastolic pressure-volume relationship; therefore, a small increase in left ventricular end-diastolic volume causes a marked increase in left ventricular enddiastolic pressure. Another most common cardiac disease associated with abnormal LV diastolic function is myocardial ischemia. Relaxation of the ventricles involves the active transport of calcium ions into the sarcoplasmic reticulum, which allows the dissociation of myosin-actin crossbridges. Myocardial ischemia deprives the system of adequate adenosine |
triphosphate, which in turn inhibits the dissociation process
by altering the balance of the adenosine triphosphate to
adenosine diphosphate ratio, which may contribute to diastolic
dysfunction18.
The heart rate determines the time that is available for
diastolic filling, coronary perfusion and ventricular relaxation.
In DHF, increase in cardiac output relatively depends upon
heart rate but a rapid heart rate may further elevate abnormal
LV filling pressures. Tachycardia adversely affects diastolic
function by several mechanisms: it decreases left ventricular
filling and coronary perfusion times, increases myocardial
oxygen consumption and causes incomplete relaxation
because the stiff heart cannot increase its velocity of relaxation
as heart rate increases. In effect, the ventricle may never fully
relax to receive blood adequately. Similiarly atrial fibrillation
completely eliminates the late diastolic atrial contribution to
LV filling, upon which patients with diastolic dysfunction
are dependent, often precipitating pulmonary edema.
Diastolic dysfunction is more common in elderly persons,
partly because of increased collagen cross-linking, increased
smooth muscle content and loss of elastic fibers19,20. These
changes tend to decrease ventricular compliance it making
more susceptible to the adverse effects of hypertension,
tachycardia and atrial fibrillation.
DIAGNOSIS OF DHF
The Working Group for the European Society of Cardiology
proposed that diagnosis of DHF requires three obligatory
diagnostic criteria to be simultaneously satisfied21:
i) signs and symptoms of congestive heart failure;
ii) normal or mildly abnormal systolic LV systolic function
and
iii) evidence of LV diastolic dysfunction (abnormal LV
relaxation, filling, diastolic distensibility or diastolic
stiffness)
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| Figure.2. Pulse Wave Pattern: Disease Progression of Left Ventricular Diastolic Dysfunction. |
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2. Normal or mildly abnormal systolic left ventricular function The presence of normal or mildly abnormal systolic LV function constitutes the second criterion for the diagnosis of heart failure (HF) with normal left ventricular ejection fraction (LVEF) - HFNLVEF. In the present consensus document, an
LVEF > 50% is also considered consistent with the presence of normal or mildly abnormal systolic LV function 22-24. LVEF needs to be assessed in accordance to the recent recommendations for cardiac chamber quantification of the American Society of Echocardiography and the European
Association of Echocardiography25. It is of importance to note that in DHF reduced long-axis shortening is frequently compensated for by increased short-axis shortening. As already demonstrated by Frank, Starling, and Wiggers and later re-appraised26, LV relaxation depends on endsystolic load and volume27-31. The criterion of presence of normal or mildly abnormal LV function therefore needs to be
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| Figure.3. Left Ventricular Inflow Color Doppler at the level of Mitral leaflet tip. Normal E/A: 1-2, Normal DT: 150-200 msec. |
implemented with measures of LV volumes. To exclude
significant LV enlargement25, LVEDVI and LV end-systolic
volume index cannot exceed 97 mL/m2 and 49 mL/m2,
respectively. 3. Evidence of LV diastolic dysfunction Conventional Doppler assessment of LV diastolic dysfunction Mitral inflow measurements which included peak early (E) and peak late (A) flow velocities, the E/A ratio, the deceleration time of early mitral flow velocity (DT), the isovolumetric relaxation time (IVRT) at rest and during the Valsalva |
TISSUE DOPPLER ASSESSMENT OF LV
DIASTOLIC DYSFUNCTION
Tissue Doppler (TD) echocardiography helps to accurately quantify LV diastolic function. TD may be used to quantify myocardial velocities in multiple segments of the myocardium from different echocardiographic acoustic windows. The most frequently used modality of TD is measurement of LV basal (annular), longitudinal myocardial shortening, or lengthening velocity. Measurements can be obtained either at the septal or at the lateral side of the mitral annulus. The peak systolic (S) shortening velocity and the early diastolic (E′) lengthening velocities are considered to be sensitive measures of LV systolic or diastolic function. Especially, the ratio of early mitral valve flow velocity (E) divided by E′ correlates closely with LV filling pressures. E depends on left atrial driving pressure, LV relaxation kinetics, and age but E′
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| Figure.4. Tissue Doppler Imaging of various Left Ventricular wall segments. |
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conceptualized as the amount of blood entering the LV during early filling, whereas E represents the gradient necessary to make this blood enter the LV. A high E/E′ thus represents a high gradient for a low shift in volume. Information on LV filling pressures can also be derived from the time interval between the onset of E and the onset of E′ (TE-E′)32,33. When the ratio E/E′ exceeds 15, LV filling pressures are elevated and when the ratio is lower than 8, LV filling pressures are low34. E/E′ is a powerful predictor of survival after myocardial infarction and E/E′>15 is superior as predictor of prognosis than clinical or other echocardiographic variables35. The close correlation between E/E′ and LV filling pressures has been confirmed in heart failure patients with depressed (< 50%) or preserved LV ejection fraction36 and in patients with slow relaxation or pseudonormal early mitral valve flow velocity filling patterns37. In the diagnostic flow charts shown in Figure 5, the ratio E/E′ is therefore considered diagnostic evidence of presence of diastolic LV dysfunction if E/E′ > 15, and diagnostic evidence of absence of HFNLVEF if E/E′ < 8. An E/E′ ratio ranging from 8 to 15 is considered suggestive but nondiagnostic evidence of diastolic LV dysfunction and needs to be implemented with other non-invasive investigations. Invasive method of assessment of LV diastolic dysfunction Definite evidence of abnormal LV relaxation, filling, diastolic
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| Figure 6. Comparison between Mitral Flow Doppler and Mitral Annular Velocity (TDI). |
distensibility or diastolic stiffness can be acquired invasively
during cardiac catheterization21, 23,24,37. Such evidence consists
of a time constant of LV relaxation (τ) > 48 ms, an LV enddiastolic
pressure > 16 mmHg or a mean pulmonary capillary
wedge pressure > 12 mmHg38-41. A diastolic LV stiffness
modulus > 0.27 also provides diagnostic evidence of diastolic
LV dysfunction.
It has been pointed out that mitral flow Doppler alone, with
its 40% to 70% specificity, cannot reliably detect diastolic
dysfunction in HFNLVEF42-44. TDI including the transmitral
flow velocity to annular velocity ratio (E/E′index)43,45, which
measures myocardial velocities during the cardiac cycle, is
considered more reliable for diagnosing diastolic dysfunction.
Oh et al46 proposed comprehensive Doppler echocardiography
with color flow or TDI as the most practical and reproducible
method for either confirming or excluding diastolic
dysfunction in HFNLVEF. In contrast, Maurer et al47 recently |
| Figure 5. Diagnostic algorithm on “DHF”. LVEDVI, left ventricular end-diastolic volume index; PCWP, mean pulmonary capillary wedge pressure; LVEDP, left ventricular end-diastolic pressure; TDI, tissue Doppler Imaging; E, early mitral valve flow velocity; E' early TD lengthening velocity; BNP, brain natriuretic peptide; E/A, ratio of early (E) to late (A) mitral valve flow velocity; DT, deceleration time; LVMI, left ventricular mass index; LAVI, left atrial volume index; Ard, duration of reverse pulmonary vein atrial systole flow; Ad, duration of mitral valve atrial wave flow. |
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argued that Doppler-derived diastolic parameters do not
provide specific information on intrinsic passive diastolic
properties and thus that diastolic dysfunction cannot be
diagnosed by Doppler echocardiography. Invasive
measurement of pressure–volume (PV) relationships with a
conductance catheter system is generally considered most
accurate for characterizing diastolic cardiac function48. It
allows direct detection of LV relaxation abnormalities and
passive LV stiffness characterized by a change in diastolic
LV pressure relative to diastolic LV volume. A recent study
Mario Kasner et al49 was the first to investigate the accuracy
of several echocardiographic Doppler techniques in detecting
diastolic dysfunction in HFNLVEF by direct comparison
with invasive PV loop data. It was found that no diastolic
index of conventional Doppler echocardiography alone was
sufficient to make the correct diagnosis. These indices
correlated only weakly with diastolic relaxation anomalies
and not at all with the degree of LV stiffness. On the other
hand, TDI investigations and the LV filling index E/E′ lat
were well suited for detecting invasively proven diastolic
dysfunction in HFNLVEF patients.
NEW MODALITIES FOR ASSESSMENT
OF LV DIASTOLIC DYSFUNCTION
Many studies have shown that atrial function is particularly
important when ventricular dysfunction exists. Kurt et al50
has shown that evaluation of LA systolic and diastolic function
using strain Doppler echocardiography has reasonably high
accuracy. This study showed that patients with DHF have a
significantly reduced LA strain and strain rate during LV
systole and increased LA stiffness index. Increased LA
stiffness as assessed invasively and noninvasively readily
identify patients with DHF from those with LV diastolic
dysfunction. On the other hand, LV mass, volumes, and
systolic function, LA volumes and atrial pump function were
not significantly different in the patients of DHF and LVDD.
LA strain and strain rate
Strain and strain rate (SR) echocardiography are new emerging
real time ultrasound techniques that provide a measure of
wall motion or a measure of deformation. Radial and
longitudinal atrial or ventricular function can be assessed by
the analysis of wall deformation using the rate of deformation
of a myocardial segment (strain rate) and its deformation
over time (strain). A negative strain rate corresponds to
myocardial shortening or thickening, whereas a positive
strain rate corresponds to myocardial lengthening or thinning.
Atrial strain and strain rate measurements are usually obtained
during ventricular and atrial systole using sample volumes
placed in the atrial myocardium near but clearly superior to
the mitral annulus. For LA “diastolic” strain variables (during
dysfunction. LA stiffness index Stiffness is conventionally defined as the force required to displace a passive spring a unit length. Physiologically it is the change in pressure required to increase the volume of a passive container a unit amount. LA stiffness can be estimated invasively i.e by ratio of pulmonary wedge pressure to LA systolic strain and noninvasive LA stiffness can be calculated by ratio of E/E′ & LA strain. LA systolic strain is determined by averaging values from four sites in the LA myocardium. The units of LA stiffness are mmHg. Importantly, the denominator in this expression, although measured in the LA wall, is determined primarily by longitudinal apically directed displacement of the mitral annulus by the contracting ventricle, whereas the posterior aspect of the LA remains fixed. Hence this index, usually attributed to the LA as a stiffness measure, is very strongly influenced by LV properties. LA stiffness as assessed invasively and noninvasively readily identified patients with DHF from those with LV diastolic dysfunction. Kurt et al50 has shown that a LA stiffness index of > 1.1 mm Hg had a sensitivity of 84%, and a specificity of 100% in distinguishing patients with DHF from those with LV diastolic dysfunction. Using E/E′ ratio in lieu of PCWP was also accurate in identifying DHF patients and an index of 0.99 had
a sensitivity of 85% and a specificity of 78% in distinguishing patients with DHF from those with LV diastolic dysfunction. Left atrial volume measurements A left atrial volume indexed to body surface area (left atrial volume index) > 32 mL/m2 was first recognized in the elderly as a strong predictor (p = 0.003) of a cardiovascular event with a higher predictive value than other echocardiographically derived indices such as LV mass index (p = 0.014) or LV diastolic dysfunction (p = 0.029)51.
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In a population-based study, left atrial volume index was also
strongly associated with the severity and duration of diastolic
LV dysfunction: the left atrial volume index progressively
increased from a value of 23+6 mL/m2 in normals to 25+8
mL/m2 in mild diastolic LV dysfunction, to 31+8 mL/m2 in
moderate diastolic LV dysfunction, and finally to 48+12 mL/
m2 in severe diastolic LV dysfunction52. Left atrial volume
index was therefore proposed as a biomarker of both diastolic
LV dysfunction and cardiovascular risk53,54. Left atrial volume
index (LAVi) is a more robust marker than left atrial area or
left atrial diameter55,56.
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| Figure 7. Myocardial tissue Doppler Imaging at the base of Septum. |
For these reasons, a left atrial volume index >40 mL/m2 has
been taken to provide sufficient evidence of diastolic LV
dysfunction when the E/E′ ratio is non-conclusive (i.e. 15>E/
E′>8) or when plasma levels of natriuretic peptides are
elevated. Similarly, a left atrial volume index < 29 mL/m2 is
proposed as a prerequisite to exclude HFNLVEF. Left atrial
volume index values of 29 and 40 mL/m2 correspond,
respectively, to the lower cut-off values of mildly abnormal and severely abnormal LA size in the recent recommendations for cardiac chamber quantification of the American Society of Echocardiography and the European Association of Echocardiography57. LV torsion with 2D Speckle tracking echocardiography Left ventricular torsion (LVtor) and subsequent untwisting play an important role in diastolic filling. Sung-Ji et al58 has shown that systolic torsion and diastolic untwisting are significantly increased in patients with mild diastolic dysfunction. However, analysis of LVtor with speckle tracking echocardiography needs to be further explored to elucidate the role of torsion in patients with LV diastolic dysfunction. ROLE OF BNP IN DHF Measurements of the levels of B-natreuretic peptide (BNP) |
have been used to confirm the diagnosis of heart failure59. Large population-based studies using BNP to screen for heart failure demonstrate a sensitivity of 40-50% and a specificity of 95% in detecting ejection fraction of less than 40%60. The diagnostic accuracy of BNP increases tremendously if we include diastolic heart-failure patients. Therefore, the same authors61 found that when including diastolic dysfunction on echo, BNP had a sensitivity of 91% and a specificity of 82%. Doust et al62 reviewed 20 studies looking at the accuracy of BNP in the diagnosis of heart failure and found that BNP had an area under the receiver operator curve of 0.83. Using the pooled diagnostic odds ratio (DOR) [sensitivity/(1-sensitivity)]/[(1-specificity)/ specificity] they demonstrated a DOR of 11.6 for studies that compared BNP with impaired ejection fraction and a DOR of around 30 for studies that compared BNP with clinical heart failure including patients with diastolic heart failure. Therefore, BNP’s diagnostic accuracy was increased when diastolic heart failure patients were included in the disease group. Moreover, in normal individuals, the concentration of BNP rises with age and is higher in women than in men63. BNP levels can be influenced by comorbidities such as sepsis64, liver failure65, or kidney failure66, pulmonary hypertension as a result of chronic obstructive pulmonary
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| Figure 8. Left Ventricular Strain and Strain Rate Imaging. |
disease67, pulmonary embolism68, or mechanical ventilation69
and obesity70. BNP levels are therefore recommended mainly
for exclusion of HFNLVEF and not for diagnosis of
HFNLVEF. Furthermore, when used for diagnostic purposes,
BNP levels alone does not provide diagnostic standard evidence of HFNLVEF and always need to be complemented with other echocardiographic variables. |
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As DHF accounts for 40-50% of heart failure cases and is responsible for significant mortality and morbidity, therefore the need of routine use of TDI cannot be overemphasized. However, newer modalities such as LV or LA strain & strain rate, LA ejection fraction, LA stiffness index, LAVi measurements need to be explored to enhance the potentials of therapeutic options and thereby effectively stratifying the patients of DHF & may be promising noninvasive tool for detection of early DHF. .
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