The ejection fraction (EF) in heart disease with high-dose dobutamine suggests associated coronary heart disease, and may help when selecting cases for coronary arteriography.
The association of LV hypertrophy, hypokinesia, and sometimes significant dilatation is compatible with hypertensive heart disease or end-stage hypertrophic cardiomyopathy. Hypertensive heart disease is clearly suspected when heart failure is associated with a history of hypertension. Echocardiography may show mild-to-moderate LV hypertrophy as well as normal wall thickness. LV mass is increased in both hypertensive and idiopathic LV dysfunction.
Hypertrophic cardiomyopathy may proceed with progressive dilatation, hypokinesia, and regression of the hypertrophy. Serial echocardiography is useful in distinguishing this condition from idiopathic dilated cardiomyopathy.
Restrictive cardiomyopathy is characterized by heart failure and preserved LVEF in the absence of significant ventricular dilatation and hypertrophy. Atrial enlargement and a restrictive filling pattern are typical, although not pathognomonic, features. In distinguishing constrictive pericarditis from restrictive cardiomyopathy, useful Doppler signs are wide respiratory variability in mitral and tricuspid flow velocities, due to increased ventricular interdependence caused by an abnormally rigid pericardium.
No useful echocardiographic finding differentiates patients with genetic dilated cardiomyopathy or myocarditis from those with idiopathic dilated cardiomyopathy. Clinical data, such as family history, recent influenza-like syndrome, recent heart failure onset, and systematic echocardiographic screening of family members, remain indispensable to diagnosis and further investigation (such as genetic studies and endomyocardial biopsy).
Some advanced cases of right ventricular dysplasia/cardiomyopathy may reveal biventricular involvement and mimic dilated cardiomyopathy. Echocardiography in these patients usually shows predominantly right ventricular dilatation and multiple akinetic/dyskinetic bulges in the absence of pulmonary hypertension.
The patients with significant LV dysfunction and severe valvular heart disease (such as aortic stenosis or mitral regurgitation) are very difficult to manage. In severe aortic stenosis associated with significant LV dysfunction, there is a low transvalvular gradient but a reduced functional area. In significant aortic stenosis, low-dose dobutamine increases the gradient but the functional valvular area remains decreased. In cases without significant aortic stenosis, the increased myocardial contractile function with dobutamine does not significantly increase the gradient but does increase the functional area.
Severe mitral insufficiency in the presence of significant LV dysfunction may require studies of mitral morphology (prolapse, chordae tendinae rupture) by transthoracic and transesophageal echocardiography. Anthracycline toxicity is characterized by systolic and diastolic restrictive dysfunction and even right ventricular dysfunction in some cases. Similar patterns, with or without hypertrophy, are seen in infiltrative disease such as hemochromatosis.
In tachy-cardiomyopathy, echocardiography is useful in quantifying LV dysfunction during arrhythmias and confirming the absence of LV dysfunction after sinus rhythm restoration.
This principle can be applied to calculate flows through different valves, valve areas, regurgitant volumes, shunts and cardiac output. Cardiac output is the product of stroke volume and heart rate. Stroke volume can be determined by two-dimensional echocardiography (end-diastolic volume-end-systolic volume) or by the Doppler method mentioned earlier, which can be applied to any of the cardiac valves, assuming no significant valvular regurgitation is present.
Estimation of pressures
Intravascular pressure gradients can be calculated using a modification of the Bernoulli equation, which expresses the law of conservation of energy and is given by: Pj-P2 (pressure drop)=l/2 r(V22-Vj2) + pi dv/dt ds + R(V) where P: pressure; r: density; V: velocity; P; and Vji pressure and velocity proximal to stenosis; and P2 and V2 are pressure and velocity distal to stenosis.
The terms on the right-hand side reflect convective energy, energy caused by flow acceleration, and energy due to viscosity factors, respectively. In the presence of a stenosis, convective energy becomes the major factor in the equation, and the other two components can be ignored. Furthermore, when V2 greatly exceeds Vj, as in obstruction, the pressure drop can be given by 4V22, expressing the velocity in m/s and the pressure gradient in mm Hg because the density of blood approximates to 1 g/cm3. This modified equation can be used to estimate the pressure gradients across valves and can thus be applied to derive ventricular and atrial pressures.
The principal and most accurate approach for estimating pulmonary artery pressure is based on a modified Bernoulli equation in which the tricuspid regurgitant jet is used to estimate pulmonary artery systolic pressure and the pulmonary regurgitation jet is used to estimate pulmonary artery mean and diastolic pressures. Peak velocity across the tricuspid valve in systole can be determined using continuous-wave Doppler. With the modified Bernoulli equation, the velocity can be converted to a pressure gradient; the right ventricular (RV) systolic pressure is given by tricuspid pressure gradient plus right atrial (RA) pressure. In the absence of pulmonary stenosis, the RV systolic pressure equals the pulmonary artery (PA) systolic pressure.
Likewise, the end-diastolic velocity of the pulmonary regurgitant jet maybe used to estimate the PA diastolic pressure, whereby the end-diastolic velocity of the pulmonary regurgitation jet equals the pressure gradient between the PA and RV at end-diastole. The PA diastolic pressure can be given by the end-diastolic pulmonary gradient plus RA pressure.
The mean PA pressure can be derived as the gradient calculated from the peak velocity of the pulmonary regurgitation jet, assuming that the RV early diastolic pressure is close to zero. It can also be calculated as:
PA diastolic pressure + 1/3 (PA systolic – PA diastolic pressure).
In pulmonary hypertension, the acceleration time (AcT), which is measured from onset of flow to peak systolic flow, is shortened and therefore can be applied to estimate the mean PA pressure using regression equations. A flat interventricular septum in systole and diastole indicates significant pulmonary hypertension.
Estimation of left ventricular filling pressures
Doppler recordings of mitral and pulmonary venous flow have been used to estimate filling pressures with great success in the presence of LV systolic dysfunction. Early diastolic flow and velocity are directly related to left atrial (LA) v-wave pressure and are inversely related to the LV diastolic pressure. In the presence of impaired relaxation, LV diastolic pressure is abnormally elevated and consequently early diastolic velocity is reduced. Given the incomplete emptying of the left atrium in early diastole, precontraction atrial volume becomes increased. According to the Frank-Star-ling law, this increased atrial stretch leads to increased atrial contraction and therefore emptying in late diastole, resulting in a prominent A wave. Such an inflow pattern is described as impaired relaxation.
In addition to the reduced E-to-A ratio, and prolonged AcT and deceleration time DT of the E velocity, the mitral valve opens after a longer isovolumic relaxation time. To maintain stroke volume, LA pressure increases, and with it the transmitral pressure gradient. Accordingly the E velocity, and its acceleration and deceleration rates, increase so that the inflow pattern shows an increased E-to-A ratio, shorter AcT and DT, a reduced atrial filling fraction, and a shorter isovolumic relaxation time. This inflow pattern is described as pseudonormal. These changes subsequently become accentuated with the development of a restrictive inflow pattern. Pulmonary venous flow can also be analyzed to derive the LV filling pressures. Forward flow into the left atrium from the pulmonary veins occurs in systole and diastole. After atrial contraction, retrograde flow (Ar) into the veins from the left atrium is observed. As the LA pressure increases, the systolic velocity of the pulmonary venous flow is reduced, with a predominance of diastolic flow. This happens because the atrium empties in diastole and therefore has a lower pressure in relation to the pulmonary veins at that time. Ar velocity and duration also provide a reasonable measure of filling pressures. As these increase, both the velocity and duration of Ar increase. With a stiff LV, atrial contraction results in antegrade flow across the mitral valve of short duration, and an Ar of longer duration into the pulmonary veins (a positive Ar-A duration). This parameter has proved the best predictor of elevated LV end-diastolic pressure in patients with normal systolic function.
Left atrial volumes can also be used to predict filling pressures with larger maximal and minimal volumes and lower atrial emptying fractions in patients with elevated filling pressures.
Two new indices of LV relaxation seem to be less load-dependent than the conventional parameters: (i) the flow propagation velocity of the E velocity into the LV as recorded by color M-mode; and (ii) the early diastolic mitral annular recoil velocity, as recorded by tissue Doppler. The ratio of the mitral E velocity to the early diastolic propagation velocity or to recoil velocity provides a reasonable estimate of LV filling pressures.
Estimation of mean right pressure
An indirect approach involves inferior vena cava size and its change with respiration. Patients with markedly elevated right atrial pressure usually have a dilated vena cava that changes minimally with respiration. Another approach involves recording and measuring hepatic venous flow. With increasing right atrial pressure, antegrade systolic venous flow decreases, whereas antegrade diastolic flow increases; thus the proportion of right atrial filling during systole decreases. Also the atrial reversal wave in the hepatic veins caused by atrial contraction increases in duration.
Determination of prognosis
It is important to be able to stratify heart failure patients into risk groups for early death if we are to improve the targeting of heart transplantation or aggressive medical treatment. Vitarelli and Gheorghi-ade calculated the predictors of cardiac death in heart failure (Table II):
instrumental finding; echocardiography; left ventricular function; cardiomyopathy; hemodynamics; blood flow; pressure; left ventricular filling pressure; prognosis