Hemodynamic Diagnosis of Ventricular Interdependence in Patients with Heart Failure in the Cardiac Catheterization Laboratory

Hemodynamic Diagnosis of Ventricular Interdependence in Patients with Heart Failure in the Cardiac Catheterization Laboratory

S112 Journal of Cardiac Failure Vol. 11 No. 6 Suppl. 2005 084 086 Ventricular Pump Function in Patients with Heart Failure: Stroke Work and Its Re...

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S112

Journal of Cardiac Failure Vol. 11 No. 6 Suppl. 2005

084

086

Ventricular Pump Function in Patients with Heart Failure: Stroke Work and Its Relation to Myocardial Mass Mathew S. Maurer1, Raja Wajahat1, Donald L. King1, Daniel Burkhoff1; 1Medicine, Columbia University, New York, NY

Heterogeneity of In Vitro Myocardial Mechanics in Amyloidosis Rebecca E. Petre1, Michael P. Quaile1, Bruce Goldman2, Steven R. Houser1, Kenneth B. Margulies3; 1Dept of Physiology/Cardiovascular Research Center, Temple U School of Medicine, Philadelphia, PA; 2Dept of Pathology, Temple U School of Medicine, Philadelphia, PA; 3Dept of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA

Background: Ventricular pump function depends on both systolic and diastolic properties. Simultaneously measuring the end systolic and end diastolic pressure volume relation (ESPVR and EDPVR) and quantifying the difference between them can facilitate conclusions about the presence and mechanisms of hemodynamic abnormalities in patients with heart failure (HF). Stroke work (SW) is one method used to quantify the area between the ESPVR and the EDPVR. We evaluated the SW and SW normalized for myocardial mass in healthy subjects and those with HF from diverse causes to evaluate ventricular performance. Methods: We studied: (1) healthy controls (n ⫽ 66, EF ⫽ 56 ⫾ 4), and patients with (2) systolic heart failure (SHF;n ⫽ 32, EF ⫽ 24 ⫾ 7) and (3) heart failure with a normal EF (HFNEF; n ⫽ 83, EF ⫽ 53 ⫾ 5). The latter group included two subgroups: (a) non-hypertensive HFNEF subjects including idiopathic hypertrophic cardiomyopathy (n ⫽ 7), restrictive cardiomyopathy (n ⫽ 4), acromegaly (n ⫽ 4) and infiltrative cardiac diseases (amyloidosis and iron overload; n ⫽ 14) and (b) hypertensive subjects with HFNEF (HTN⫹HFNEF, n ⫽ 54). Freehand 3D echocardiography was performed to measure ventricular volumes and mass. SW was calculated as MAP*SV and indexed to myocardial mass. Results: Subjects with HTN⫹HFNEF were older women while subjects with nonhypertensive HFNEF were younger. LV Mass was increased in all HF cohorts with concentric hypertrophy in non-hypertensive HFNEF and eccentric hypertrophy in SHF. SW was significantly increased in the HTN⫹HFNEF cohort. SW/LV mass was significantly decreased in the SHF and non-hypertensive HFNEF cohorts while remaining normal in HTN⫹HFNEF. Conclusions: Ventricular pump function is decreased in subjects with SHF and non-hypertensive HFNEF but subjects with HTN⫹ HFNEF have increased stroke work that is commensurate with their increased LV mass. These data suggest that pump function does not differ from normal in hypertensive HFNEF.

Parameter Age (years) Gender (% female) SBP (mm Hg) DBP (mm Hg) LV mass (grams) EDV/LV Mass (ml/gm) Stroke Work (ml*mm Hg) SW/Mass (ml*mmHg/grams)

Systolic Heart Non-Hypertensive Hypertensive Failure HFNEF HFNEF

Normals 55 ⫾ 20 53% 120 ⫾ 25 71 ⫾ 16 136 ⫾ 25

62 ⫾ 15 25%* 108 ⫾ 26 67 ⫾ 15 259 ⫾ 76*

0.77 ⫾ 0.12

0.93 ⫾ 0.20*

0.66 ⫾ 0.20*

0.70 ⫾ 0.18

9686 ⫾ 2593 8312 ⫾ 3970

8962 ⫾ 2762

12283 ⫾ 3877*

53 ⫾ 19*

71 ⫾ 18

71 ⫾ 12

33 ⫾ 14*

43 ⫾ 20* 52% 116 ⫾ 10 66 ⫾ 10 179 ⫾ 45*

71 ⫾ 15* 74%* 146 ⫾ 23* 74 ⫾ 11 176 ⫾ 47*

*p ⬍ 0.05 compared with normals

085 Hemodynamic Diagnosis of Ventricular Interdependence in Patients with Heart Failure in the Cardiac Catheterization Laboratory Theo Meyer, Cynthia Ennis, Stephanie Moore, Stephanie Ennis; Medicine, Division of Cardiology, University of Massachusetts Medical Center, Worcester, MA Background: Because of close anatomic association, the pressure and volume in the right ventricle (RV) can directly influence the pressure and volume in the left ventricle (LV). This phenomenon is termed ventricular interdependence (VI), and is the hemodynamic hallmark of constrictive pericarditis. VI is also found in patients with severe heart failure. In heart failure patients in whom VI is evident, LV filling pressure is more a reflection of right-sided diastolic pressures than of LV volume. This is particularly evident in patients with RV pressure and volume overload. In some instances LV stroke volume may increase as filling pressure is reduced. The demonstration of VI in heart failure patients in the cardiac catheterization laboratory may have clinical relevance. This study examined the utility of three hemodynamic indexes to diagnose VI in heart failure patients. Methods and Results: Hemodynamic criteria used to demonstrate VI included: a)equilibration of intracardiac pressures (EP), enhanced discordance between RV and LV systolic pressures during inspiration (RVindex), and LV and RV pressure response to abdominal compression (AC-VI). The latter relies on demonstrating an immediate and parallel increase in RV and LV diastolic and systolic pressures during AC followed by an immediate and simultaneous decline in RV and LV diastolic and systolic pressures during release of AC. Fluidfilled catheters were used to study 24 patients: 7 patients with constrictive pericarditis (Control group-classical hemodynamic model of VI) and 18 patients with other causes of severe heart failure (HF group). VI was demonstrated in 8 patients in HF group. RV dilation, as shown by echocardiography, was present in 75% of these patients. Nearly 60% of these patients showed improvements in their creatinine concentrations with vigorous diuresis. Unloading of the RV may have resulted in improved LV filling and cardiac output. The frequency of hemodynamic indexes of VI is shown in the Table. Conclusion: 1.0 VI is relatively common in patients with severe heart failure referred for cardiac catheterization. 2.0 AC-VI provides the most reproducible and reliable index of VI in patients with severe heart failure undergoing cardiac catheterization.

EP RV-index AC-VI

Control Group (n ⫽ 7)

Hf Group (n ⫽ 8)

71% 51% 100%

75% 63% 100%

Amyloidosis is a condition in which there is accumulation of amyloid, an insoluble protein, in various organs of the body. Cardiac amyloidosis has been associated with abnormalities in both contractility and diastolic stiffness. We speculated that regional variability in amyloid deposition might provide an opportunity to examine the relative balance between abnormalities in contractility and stiffness. Methods: At the time of cardiac transplantation, free running, isolated trabeculae were dissected from the native right ventricular myocardium of a 59 year-old female with inotrope-dependent cardiac amyloidosis (LVEF 10–15%). Isometric force transients were measured at various lengths (20, 40, 60, 80, 100 % Lmax) in nine trabeculae. The slope of active and passive length-tension relationships were used to define contractility and stiffness. Several trabeculae and tissue samples were preserved in 4% paraformaldehyde, embedded, sectioned, and stained with either crystal violet (CV) or immunostained for SAA protein to identify the proportion of tissue infiltrated with amyloid. Results: We observed varying degrees of abnormal contractility and stiffness in these trabeculae. The most common pattern (n ⫽ 4) was severely depressed contractility with markedly increased stiffness (Figure A; -o- represents diastolic force, -♦- represents developed force). However, three trabeculae demonstrated normal stiffness with severely decreased contractility, one demonstrated relatively intact contractility despite severely increased stiffness (Figure B), and one had normal contractility and normal stiffness. Conclusion: Even within the subendocardium of a single heart, there is substantial regional variability of amyloid deposits and substantial variability in the biomechanical defects associated with amyloidosis. These data also illustrate that even in myocardium with an intact Frank-Starling mechanism, marked increases in stiffness can effectively preclude utilizing this source of contractile reserve in vivo.