Wide-range load shift of combined aortic valvuloplasty-arterial vasodilation slows isovolumic relaxation of the hypertrophied left ventricle.

Paulus, Walter J.; Heyndrickx, Guy R.; Buyl, P; Goethals, Marc; Andries, Erik

doi:10.1161/01.cir.81.3.886

Cited by 13 publications

(3 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…15 The average increase of 7 mmHg in RV systolic pressure, however, is too small to explain the prolonged isovolumic pressure decay in HCM patients with normal systolic function. 14,16,18 In fact, we also observed a prolongation of the time constants of relaxation in HCM patients when compared to HCM patients in whom RV systolic pressure did not exceed 30 mmHg and with normal subjects (HCM: 27±5 mmHg; N: 23±3 mmHg, NS).…”

Section: Rv Relaxationsupporting

confidence: 49%

Right Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

1999

View full text Add to dashboard Cite

ypertrophic cardiomyopathy (HCM) is hemodynamically characterized by abnormal ventricular diastolic function: impaired isovolumic relaxation, 1-4 abnormal diastolic filling pattern, [3][4][5][6] and decreased diastolic distensibility. 3,4 These abnormalities have been well demonstrated in the left ventricle (LV), but little information has been available concerning the right ventricle (RV) in HCM patients. Suzuki et al using cine magnetic resonance imaging, showed decreased RV early diastolic filling in HCM patients. 7 However, there has been no systematic study of RV isovolumic relaxation, diastolic filling, or compliance in HCM patients, because invasive studies are needed to analyze high-fidelity ventricular pressures and volumes.The purpose of the present study was to systematically investigate RV isovolumic relaxation, diastolic filling, and diastolic distensibility in HCM patients and to compare those variables with other hemodynamic variables and those of the LV. We did this by analyzing high-fidelity RV and LV pressures using catheter-tipped manometers and biplane RV cine-angiograms in HCM patients. Methods Study SubjectsThe study group comprised 19 patients with HCM and a control group of 13 patients investigated for chest pain who proved to have angiographically normal coronary arteries and normal LV function. The HCM patients were 18 men Japanese Circulation Journal Vol.63, September 1999 and 1 woman with an average age of 45 years (range, 20-60 years). Among the normal control subjects were 7 men and 6 women with an average age of 50 years (range, 36-72 years). The diagnosis of HCM was made by clinical, echocardiographic, and angiographic evaluation. Based on the echocardiographic classification, all patients had asymmetrical septal hypertrophy with a septal-to-posterior wall ratio of 1.3:1 or more. The thickness of the interventricular septum and posterior free wall was 20.5±4.5 and 12.2±2.6 mm, respectively. All patients had normal sinus rhythm. No patient with HCM had a resting RV or LV outflow tract pressure gradient. Patients with apical hypertrophic cardiomyopathy were not included in this study. All medications, including calcium antagonists, were terminated at least 5 days before cardiac catheterization. Informed consent was obtained from each patient, and there were no complications as a result of this study. Study ProtocolCardiac catheterization was performed via the percutaneous femoral approach in the fasting state. RV and LV pressures were measured using a catheter-tip manometer (RV: Goodtec, USA; LV: Millar Instruments, Houston, TX, USA) and recorded at a paper speed of 150-200 mm/s (Electronics for Medicine VR-12, Pleasantville, NY, USA). After routine right and left heart catheterization, we inserted another catheter via the femoral vein to perform right ventriculograms. Simultaneous biplane cineventriculograms were obtained in the 30°right anterior oblique and 60°left anterior oblique projections by injecting 40 ml of iohexol at a rate of 10-12 ml/s. The film speed was 50 frames/s...

show abstract

Section: Rv Relaxationsupporting

confidence: 49%

Right Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

1999

View full text Add to dashboard Cite

show abstract

“…20 The radial myocardial stiffness modulus (E) was calculated to assess myocardial material properties from the formula: Eϭ⌬ R / ⌬⑀ R ϭ⌬P/(⌬h/h)ϭϪ⌬P/⌬ln h and assuming the increment in radial stress (⌬ R ) to be equal but opposite in sign to the increment in ⌬P at the endocardium and the increment in radial strain (⌬⑀ R ) to be equal to the increment in wall thickness (⌬h) relative to the instantaneous wall thickness. Because ⌬h/hϭ⌬ln h, E equals the slope of a P versus ln h plot.…”

Section: Discussionmentioning

confidence: 99%

Cardiomyocyte Stiffness in Diastolic Heart Failure

Borbély¹,

Velden²,

Papp³

et al. 2005

Circulation

464

386

View full text Add to dashboard Cite

Background-Heart failure with preserved left ventricular (LV) ejection fraction (EF) is increasingly recognized and usually referred to as diastolic heart failure (DHF). Its pathogenetic mechanism remains unclear, partly because of a lack of myocardial biopsy material. Endomyocardial biopsy samples obtained from DHF patients were therefore analyzed for collagen volume fraction (CVF) and sarcomeric protein composition and compared with control samples. Single cardiomyocytes were isolated from these biopsy samples to assess cellular contractile performance. Methods and Results-DHF patients (nϭ12) had an LVEF of 71Ϯ11%, an LV end-diastolic pressure (LVEDP) of 28Ϯ4 mm Hg, and no significant coronary artery stenoses. DHF patients had higher CVFs (7.5Ϯ4.0%, PϽ0.05) than did controls (nϭ8, 3.8Ϯ2.0%), and no conspicuous changes in sarcomeric protein composition were detected. Cardiomyocytes, mechanically isolated and treated with Triton X-100 to remove all membranes, were stretched to a sarcomere length of 2.

show abstract

“…In eight patients (Table 1, patients [21][22][23][24][25][26][27][28], a 5-min intracoronary infusion of substance P (20 pmol/min) was performed (13). Substance P causes receptor-mediated coronary endothelial release of NO.…”

Section: Methodsmentioning

confidence: 99%

Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy

Bronzwaer

Heymes

Visser

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

. Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy. Am J Physiol Heart Circ Physiol 284: H10-H16, 2003; 10.1152/ajpheart.00401.2002.-The purpose of the study was to investigate interactions between myocardial nitric oxide synthase (NOS) and myocardial fibrosis, both of which determine left ventricular (LV) preload reserve in patients with nonischemic dilated cardiomyopathy (DCM). In previous animal experiments, chronic inhibition of NOS induced myocardial fibrosis and limited LV preload reserve. Twenty-eight DCM patients underwent LV catheterization, balloon caval occlusions (BCO; n ϭ 8), intracoronary substance P infusion (n ϭ 8), and procurement of LV endomyocardial biopsies for determinations of collagen volume fraction (CVF), of gene expression of NOS2, NOS3, heme oxygenase (HO)-1, and TNF-␣, and of NOS2 protein. CVF was unrelated to the intensity of NOS2, NOS3, HO-1, or TNF-␣ gene expression or of NOS2 protein expression. Preload recruitable LV stroke work (PR-LVSW) correlated directly with NOS2 gene expression (P ϭ 0.001) and inversely with CVF (P ϭ 0.04). High CVF (Ͼ10%) reduced baseline LVSW and PR-LVSW at each level of NOS2 gene expression. In DCM, myocardial fibrosis is unrelated to the intensity of myocardial gene expression of NOS, antioxidative enzymes (HO-1), or cytokines (TNF-␣) and blunts NOS2-related recruitment of LV preload reserve. collagen; diastole; myocardial contraction HIGHER LEFT VENTRICULAR (LV) endomyocardial nitric oxide (NO) synthase (NOS) gene expression enables patients with dilated cardiomyopathy (DCM) to recruit LV preload reserve as evident from their higher LV stroke work (LVSW) at elevated LV filling pressures (13). This ability to recruit LV preload reserve could result from an acute direct myocardial action of NO, because intracoronary infusion of substance P, which releases NO from the coronary endothelium, induces an instantaneous increase in LVSW in DCM patients with elevated LV filling pressures (13). This increase in LVSW is accompanied by a rightward shift of the diastolic LV pressure-volume relation. A similar NOrelated rightward shift of the diastolic LV pressurevolume relation was previously observed in control and aortic stenosis patients after intracoronary infusion of a NO donor (20,24) and in DCM patients after intracoronary infusion of enalaprilat (37). Acute effects of NO on myocardial diastolic distensibility have also been reported in experimental preparations. In isolated rat cardiomyocytes, exposure to cGMP, the second messenger of NO, increases diastolic cell length (32), and, in isolated guinea pig hearts, a coronary perfusate containing a specific NOS inhibitor results in an acute reduction of LV stroke volume because of a leftward shift of the diastolic LV pressure-volume relation (27).The ability of NO to preserve LV diastolic distensibility could result not only from its acute direct myocardial actions but also from chronic effects on LV hypertrophy and on collagen turnover within the cardiac i...

show abstract

Wide-range load shift of combined aortic valvuloplasty-arterial vasodilation slows isovolumic relaxation of the hypertrophied left ventricle.

Cited by 13 publications

References 61 publications

Right Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

Right Ventricular Diastolic Function in Patients With Hypertrophic Cardiomyopathy

Cardiomyocyte Stiffness in Diastolic Heart Failure

Myocardial fibrosis blunts nitric oxide synthase-related preload reserve in human dilated cardiomyopathy

Contact Info

Product

Resources

About