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J Am Coll Cardiol, 2008; 51:2107-2115, doi:10.1016/j.jacc.2007.12.060
© 2008 by the American College of Cardiology Foundation
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Transseptal Left Heart Catheterization

A 50-Year Odyssey

John Ross, Jr, MD, MACC*

University of California San Diego, School of Medicine, La Jolla, California.


Figure 1
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Figure 1 Original Transseptal Equipment for Human Use

(A) Cournand catheter (with removeable hub) through which the needle is inserted. The transseptal needle has a specified curve and bevel, with an attached arrow-handle for controlled rotation (B and D). The 17-gauge needle allows passage of a small catheter (C) for pressure measurements in the left atrium and left ventricle, and injection of indicator dye into the left ventricle with brachial arterial sampling, for calculation of the cardiac output. Reprinted with permission from Ross et al. (5).

 

Figure 2
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Figure 2 Left Atrial Injection of Contrast Medium Via the Transseptal Needle

Angiogram of the normal canine left heart shows left atrium (top), left ventricular diastole (center) and systole (bottom). Reprinted with permission from Ross (3).

 

Figure 3
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Figure 3 Transseptal Needle Puncture of the LA in the First Patient

Pressure tracing shows severe mitral regurgitation evidenced by giant V waves on the left atrial pressure tracing; pressure was also recorded as the needle was withdrawn from the left atrium (LA) across the interatrial septum into the right atrium (RA), where the pressure was normal. Reprinted with permission from Ross et al. (4).

 

Figure 4
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Figure 4 Pullback Tracing From LV to LA Obtained With the Small Plastic Catheter

The patient had mitral stenosis with atrial fibrillation, and the left atrial (LA) tracing shows a pattern typical of mitral stenosis, with a delayed downslope of the V-wave and a large pressure gradient across the mitral valve. Reprinted with permission from Ross et al. (5). LV = left ventricle.

 

Figure 5
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Figure 5 Transseptal Equipment Modified for Percutaneous Use

The straight stylet (B) is used for insertion of the curved transseptal catheter (A) from the femoral vein into the right atrium. The modified transseptal needle (C) has a 21-gauge needle tip to reduce hazard from accidental puncture of the aorta or atrial wall, and the catheter (E) has side holes (to enhance injection of contrast medium) and a tapered tip to facilitate entry into the femoral vein and traversal of the atrial septum. (D) Detail of transseptal needle tip. Reprinted with permission from Brockenbrough et al. (9).

 

Figure 6
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Figure 6 Responses to Graded Doses of Angiotensin II in Patients Without (Groups 1 and 2) and With Heart Failure (Group 3)

The upper panel shows changes in the stroke work index (SWI) plotted versus the left ventricular end-diastolic (LVED) pressure. The lower panel shows changes in the stroke volume index (SVI) plotted versus the LV systolic pressure in the same groups of patients. Reprinted with permission from Ross and Braunwald (14). For discussion of groups and responses see text.

 

Figure 7
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Figure 7 LV Pressure-Volume Diagrams in the Normal Heart

In the baseline pressure-volume loop (1), the stroke volume (SV) is indicated, and the arrow indicates the ejection portion of the loop. With initial induced elevation of left ventricular (LV) systolic pressure, the stroke volume decreases (loop 2), but it is restored by increased diastolic filling (loop 3). When the systolic pressure is increased after marked volume loading, the limit of pre-load reserve is reached at LV end-diastole, afterload mismatch occurs, and the stroke volume decreases (loop 4). Reprinted with permission from Ross (19).

 

Figure 8
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Figure 8 LV Wall Stress–Volume Diagrams in Heart Failure

The normal end-systolic wall stress–volume relation is represented by the dashed line, and this relation in heart failure is shifted downward with reduced slope. The resting left ventricular (LV) wall stress–volume loop in heart failure (1) shows little pre-load reserve, and increased afterload induced by angiotensin (loop 2) causes a marked decrease in the stroke volume (SV2). Administration of a vasodilator (loop 3) compared with loop 1 causes reduced afterload particularly early and late during LV ejection, an increase in stroke volume (SV3), with a modest decrease in LV end-diastolic volume. Reproduced with permission from Ross J Jr. Mechanisms of cardiac contraction: what roles for preload, afterload and inotropic state in heart failure? Eur Heart J 1983;4:19–38.

 

Figure 9
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Figure 9 LV Wall Stress–Volume Diagrams in Aortic Stenosis

The straight dashed lines show an example of the end-systolic left ventricular (LV) wall stress–volume relation in compensated aortic stenosis, with a relatively normal wall stress–volume loop (dashed loop). With LV dysfunction, the end-systolic wall stress–volume relation is shifted to the right (solid line), and the LV loop shows increased LV end-diastolic volume with marked loss of pre-load reserve, and increased systolic wall stress (the ejection fraction [EFx] is 60%, center loop solid line). With progression of aortic stenosis, afterload becomes markedly increased, pre-load reserve is lost, and the stroke volume and EFx are greatly reduced (EFx 33%). After aortic valve replacement, the post-operative loop shows reduced afterload and end-diastolic volume, and the EFx improves to 52%. Reprinted with permission from Ross (19).

 

Figure 10
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Figure 10 Wall Stress–Volume Diagram in Severe Mitral Regurgitation With Depressed Ventricular Function

Chronic volume overload shifts the wall stress–volume relation to the right, and severe myocardial depression displaces it further to the right and reduces its slope. Pre-operatively, the ejection fraction (EFx) is only slightly reduced (50%) because of the large leak into the left atrium. If the mitral valve is replaced in this setting, the EFx can decrease sharply (37%) because the weakened left ventricle must now eject entirely into the high impedance of the aorta (afterload mismatch). Reprinted with permission from Ross (19).

 

Figure 11
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Figure 11 Hemodynamic Diagnosis of Absence or Presence of Obstruction in HCM

Diagrams of the method used during transseptal catheterization to differentiate left ventricular cavity obliteration without obstruction (left panels) from true obstruction to left ventricular ejection in the outflow tract (right panels). In each case, aortic (Ao) pressure is measured and LV pressure is recorded through the transseptal catheter as it is pulled back from the left ventricular apex (position A) to the inflow tract (position B), and into the left atrium (position C). The pullback tracings below indicate cavity obliteration on the left and true obstruction on the right. Arrow in upper right figure indicates site of obstruction. Reprinted with permission from Ross et al. (24).

 

Figure 12
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Figure 12 LV Biplane Angiography in a Patient With Obstructive Hypertrophic Cardiomyopathy

(A and C) Frontal view in systole (A) and diastole (C). (B and D) Left lateral view in systole (B) and diastole (D). The positions of the aortic valve leaflets and the anterior mitral valve leaflet are indicated by dashed lines. In systole, a linear shadow is visible both in A and C, where the anterior mitral valve leaflet is apposed against the septum (arrows) in both systole and diastole. In B, the linear horizontal shadow shows the anterior leaflet positioned anteriorly against the ventricular septum during systole (arrows); mitral regurgitation is also evident. In D, the inverted cone shows the bulging interventricular septum anteriorly and the anterior mitral leaflet posteriorly. Reprinted with permission from Ross et al. (24). Ao = aorta; LA = left atrium; LV = left ventricle.

 




 
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