Echocardiographic Findings in Right Heart Disease

Right Ventricular Hypertension and Pulmonary Hypertension

As long as there is sufficient TR signal, the systolic RV–RA gradient can be calculated using the simple modified Bernouilli equation, and with the addition of an estimated mean RA pressure becomes the RVSP (which is thereby both a calculated and an estimated number). RVSP can be equated with systolic pulmonary artery pressure only when Doppler assessment of the right ventricular outflow tract and pulmonic valve excludes a gradient conferring stenosis.

It is important to recall that changes in recorded RVSP may reflect normal daily variations of pulmonary artery pressure—in a given patient, variation of up to 30% in a 24-hour period may be seen.

Echocardiography tends to overestimate lower RVSP and underestimate higher RVSP, but overall is generally accurate—as long as there is sufficient TR signal.

Older, less commonly used, echocardiographic findings that have been associated with pulmonary hypertension include the following:

Right Ventricular Hypertrophy

RV wall thickness correlates with RV systolic pressure: r = 0.92.¹

RVH is identified on echocardiography only by an increase in RV wall thickness, because an accurate calculation of RV mass is not feasible by echocardiography.

Measurement of RV wall thickness is challenging because of the exaggerated topography of the endocardial surface of the RV. Paradoxically, the better the RV endocardial detail achieved, the greater the uncertainty regarding where to measure. It is best to measure away from frank trabeculations, on whichever view gives the best detail of the RV free wall.

Normal RV wall thickness is about 3 mm on autopsy and about 4 mm (4 ± 1 mm)² by echocardiography. By convention, in the preharmonic era, RVH by echocardiography was 5 mm or greater. Thus, normal RV wall thickness and RVH are separated by only a narrow margin of 1 to 2 mm:

For the diagnosis of RVH, there is a sensitivity of 90% and specificity of 94% for diastolic wall thickness of 5 mm or greater. There is sensitivity of 34% and specificity of 100% for systolic wall thickness of 10 mm or greater.

Inferior Vena Cava Dimensions and Collapse

There is frankly poor correlation of IVC diameter with RA pressure and with RV systolic pressure r = 0.50, but the “collapsibility index” correlates somewhat better, at r = 0.71⁴:

Interventricular Septal Shape

The normal interventricular septum configuration throughout the cardiac cycle is to be concave toward the left side—i.e., in a short-axis view, the LV remains symmetrically round throughout the cardiac cycle, and any orthogonal axes (diameters) are equal in dimension, for an “eccentricity index” of 1 (D1/D2).⁵ The basis of the preservation of the roundness of the septum in both diastole and systole is the LV-to-RV pressure gradient that are normally preserved in both diastole and systole.

In RV systolic hypertension (“pressure overload”), with elevated RV systolic pressures, at end-diastole, the interventricular septum is, as it is normally, convex toward the LV. It becomes progressively flattened from end-diastole to end-systole. With suprasystemic RV systolic pressures, the interventricular septum is flattened at end-diastole and becomes concave toward the RV by end-systole.

In RV volume overload, at end-diastole, the interventricular septum is flattened toward the left side. By end-systole, the interventricular septum configuration is normal. The RV dimensions are substantially increased.⁵

Right Ventricular Volume

Determination of RV volume by echocardiography is difficult, time consuming, and not very accurate. The basic problem is the complex shape of the RV, which does not readily lend itself to reproduction with an equation, or to very reproducible measurement along arbitrary axes.

Two methods have been suggested:

It is questionable whether the time and effort to calculate RV volume by echocardiography is worthwhile, as cardiac magnetic resonance is well-suited to the task.

tricuspid annular plane excursion

Tricuspid annular plane excursion (TAPSE), measured using M-mode from an apical 4CV and describing the longitudinal excursion of the lateral tricuspid annulus, is an objective and reproducible descriptor of RV systolic function, pulmonary artery pressure, and prognosis. TAPSE correlates directly with RV ejection fraction and behaves as a linear risk variable. The mean is 23 mm, and the lower reference value (mean minus 2 standard deviations) is 16 mm. TAPSE correlates inversely with pulmonary artery systolic pressure and also inversely with prognosis in heart failure, pulmonary hypertension, and chronic obstructive pulmonary disease. Confounding aspects of the use/interpretation of TAPSE are that (1) RV longitudinal systolic function is not less well-correlated with overall RV systolic function in the presence of RV regional wall motion abnormalities, (2) LV systolic function influences overall RV systolic function via septal function, and (3) severe TR decreases the correlation of TAPSE with RV ejection fraction.

Right Ventricular Infarction

Significant RV infarction is seen predominantly in the setting of inferior infarction of the left ventricle, and rarely is seen in the absence of LV inferior and inferoseptal wall motion disturbances.

Short-axis views of the RV and LV are the most helpful. The view often must be angulated to the right side to ensure visualization of the RV, especially when the RV dilates from infarction.

The echocardiographic findings are as follows:

Complications of RV infarction that may be seen by echocardiography include the following:

Inversion of the normal curvature of the interatrial septum may be seen in the setting of RV myocardial infarction, when the RA pressure exceeds LA pressure.¹²

RVH predisposes to RV myocardial infarction in the setting of first inferior infarction, as the imbalance of supply and demand is even more unfavorable.¹³

Mid-diastolic opening of the pulmonary valve may occur after RV infarction, due to RVEDP exceeding pulmonary artery diastolic pressure before RA systole.¹⁴

Right Ventricular Dysplasia

RV dysplasia is a congenital disorder consisting of aplasia/hypoplasia with fibrofatty replacement exclusively or principally of the RV, in the presence of a structurally normal tricuspid valve. There is a spectrum of disease. Ventricular tachycardia of RV origin and right-sided heart failure are the principal consequences. The patient usually is young or middle-aged. The most severe cases occur in childhood, but milder cases may occur well into adult life. Familial cases have been described.

Although the literature reports findings of RV dysplasia as seen on echocardiography, RV dysplasia is vastly better evaluated by cardiac magnetic resonance than by echocardiography.

The following echocardiographic findings of RV dysplasia have been reported:

Pulmonary Embolism

The echocardiographic findings of PE are determined by the size and the hemodynamic burden of PE on the right heart.

With hemodynamically significant pulmonary embolism, the LV cavity (if otherwise normal) typically is small, as the pulmonary vascular obstruction results in underloading of the left heart. Doppler studies will reveal a low cardiac output, TR, and elevated RV systolic pressure. Rarely, a thrombus-in-transit has been visualized (in the IVC, RA, RV, main pulmonary artery, or branch pulmonary arteries) by transthoracic or transesophageal echocardiography.

Following lysis of the thrombus, or surgical removal, right-sided chamber dimensions and interventricular septum configuration may normalize partially or entirely.¹⁶

The role of echocardiography in the assessment of PE is unclear. It appears to provide another objective means of establishing RV strain, as do physical diagnosis findings, elevated troponins, increased RV dimensions on CT scanning, and electrocardiographic changes.

Echocardiography is only rarely able to make a direct diagnosis of PE (transesophageal echocardiographic visualization of central pulmonary artery thrombus). More commonly, echocardiography offers indirect evidence of PE by identifying RV strain features. Rarely, an embolus-in-transit is identified as a strong indirect evidence of PE. The presence of elevated RVSP is nonspecific as a sole feature and it is not adequate as an indirect sign of PE.

RV strain, identified by any modality (e.g., troponin elevation, electrocardiographic abnormalities consistent with RV strain, echocardiographic identification of RV dilation or hypokinesis) is consistent with increased clinical risk from the PE, even if BP is not reduced (submassive PE) or shocky (massive PE). Therefore, the probable role for echocardiography is to assist with stratification of risk, rather than being a diagnostic test per se.

Smaller pulmonary emboli that do not result in RV strain are exceedingly unlikely to result in abnormalities that echocardiography can identify; therefore, the sensitivity of RV echocardiographic findings of PE is heavily affected by the hemodynamic effect of the PE—in fact, it is dependent on it. The identification of emboli-in-transit is a matter of pure luck.

Primary Pulmonary Hypertension

The echocardiographic findings in primary pulmonary hypertension (PPH) are basically those of RV pressure overload, and reflect the severity of the pulmonary vascular disease. The pulmonary artery is almost invariably dilated, and pulmonary insufficiency is common. Pulmonary insufficiency, being under higher pressure than normal, is seen as being under higher velocity than normal.

The following findings augur for significantly reduced survival,¹⁷ and may be apparent by echocardiography:

A critical issue concerning echocardiography and pulmonary hypertension is that the lack of adequate TR signal (10–20% of cases) can conceal the findings of pulmonary hypertension until they are very far advanced.

BOX 23-1 Assessment Criteria and Indications for Cardiac Imaging Modalities for the Assessment of Right Heart Chamber Quantification

Transthoracic Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography¹⁸

Evaluation of Ventricular Function with TTE

Initial evaluation of ventricular function (e.g., screening) with no symptoms or signs of cardiovascular disease

Appropriateness criteria: I; median score: 2

2003 ACC/AHA Guideline Update for the Clinical Application of Echocardiography¹⁹

For pulmonary disease: pulmonary emboli and suspected clots in the right atrium or ventricle or main pulmonary artery branches^*

• Class IIa

1997 ACC/AHA Guidelines for the Clinical Application of Echocardiography²⁰

Pulmonary Disease

Suspected pulmonary hypertension

• Class I

For distinguishing cardiac versus noncardiac etiology of dyspnea in patients in whom all clinical and laboratory clues are ambiguous^*

• Class I

Follow-up of pulmonary artery pressures in patients with pulmonary hypertension to evaluate response to treatment

• Class I

Lung disease with clinical suspicion of cardiac involvement (suspected cor pulmonale)

• Class I

Measurement of exercise pulmonary artery pressure

• Class IIa

Patients being considered for lung transplantation or other surgical procedure for advanced lung disease^*

• Class IIa

Lung disease without any clinical suspicion of cardiac involvement

• Class III

Re-evaluation studies of RV function in patients with chronic obstructive lung disease without a change in clinical status

• Class III

Transesophageal Echocardiography

ACCF/ASE/AHA/ASNC/HFSA/HRS/SCAI/SCCM/SCCT/SCMR 2011 Appropriate Use Criteria for Echocardiography¹⁸

No specific entries

Cardiac Computed Tomography

ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac CT²¹

Evaluation of Ventricular Morphology and Systolic Function

Quantitative evaluation of RV function

Appropriateness criteria: A; median score 7

Assessment of RV Morphology

Suspected arrhythmogenic RV dysplasia

Appropriateness criteria: A; median score: 7²⁷

Cardiac Magnetic Resonance

ACCF/ACR/SCCT/SCMR/ASNC/NASCI/SCAI/SIR 2006 Appropriateness Criteria for Cardiac Magnetic Resonance Imaging²²

No specific entries

SCMR Consensus Indication for Cardiac Magnetic Resonance Imaging²³

For assessment of global (left and right) ventricular function

• Class I

Nuclear

ACC/AHA/ASNC 2003 Guidelines for the Clinical Use of Radionuclide Imaging²⁴

For Heart Failure: Fundamental Assessment

Initial assessment of LV and RV function at rest^*

• Test: Rest RNA

• Class I (Level of evidence: A)

Routine serial assessment of LV and RV function at rest^*

• Test: Rest RNA

• Class IIb (Level of evidence: B)

Initial or serial of ventricular function with exercise

• Test: Exercise RNA

• Class IIb (Level of evidence: B)

For valvular heart disease: initial and serial assessment of LV and RV function

• Test: Rest RNA

• Class I (Level of evidence: B)

For adults with congenital heart disease: initial and serial assessment of LV and RV function

• Test: Rest RNA

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2. Coronary Artery Disease: Ischemia, Infarction, and Complications
3. Pericardial Diseases
4. Mitral Insufficiency

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