Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study

Hanrath, Peter; Mathey, D; Siegert, R.; Bleifeld, W.

doi:10.1016/0002-9149(80)90214-3

Cited by 380 publications

(69 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Relaxation and diastolic filling of the hypertrophied left ventricle are impaired in many patients with hypertrophic cardiomyopathy.lA4 [16][17][18][19][20][21][22] Prolonged or incomplete left ventricular relaxation and subsequent reduction in the rate and the extent of rapid filling result in reduced diastolic volume, reduced stroke volume, and altered diastolic pressure-volume relationships. 16 [23][24][25][26][27] On the basis of these common physiologic abnormalities, it has been postulated, and generally accepted, that these abnormalities in left ventricular diastolic function contribute importantly to the clinical manifestations and severity of symptoms in patients with this disease.…”

Section: Discussionmentioning

confidence: 99%

Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects.

et al. 1985

View full text Add to dashboard Cite

Verapamil improves exercise tolerance and decreases symptoms in many patients with hypertrophic cardiomyopathy. The mechanisms responsible for these effects are not completely understood, although previous studies indicate that verapamil enhances left ventricular relaxation and diastolic filling in such patients. To investigate the association between changes in left ventricular filling and exercise tolerance after verapamil, we studied 55 patients with hypertrophic cardiomyopathy by radionuclide angiography and graded treadmill testing before and after 1 to 4 weeks of therapy with orally administered verapamil, 320 to 640 mg/d. The verapamil-induced increase in peak left ventricular filling rate at rest (from 3.1 ± 1.3 to 3.7 ± 1.3 end-diastolic volumes/sec; p < .001) was associated with an increase in exercise tolerance (from 5.9 ± 3.6 to 8.7 + 4.7 min; p < .001); exercise capacity increased in 34 of 43 patients (79%) manifesting an increase in peak filling rate but only one of 12 patients (8%) with unchanged or decreased peak filling rate (p < .001). This initial trend persisted in 25 patients studied after 1 year of therapy; 11 of 16 patients (69%) with a persistent increase in peak filling rate had persistent improvement in exercise tolerance relative to preverapamil values, compared with only one of nine patients (11 %) in whom peak filling rate was unchanged or decreased relative to preverapamil levels (p < .02). Verapamil withdrawal after 1 to 2 years in 24 patients resulted in reduction in peak filling rate (p < .001) and was associated with deterioration in exercise tolerance in 17 patients (71%). Hence, verapamil-induced changes in left ventricular peak filling rate were associated significantly with objective symptomatic improvement. These data support the concept that enhanced left ventricular diastolic filling is an important mechanism contributing to the clinical improvement experienced by many patients with hypertrophic cardiomyopathy during therapy with verapamil. Circulation 72, No. 4, 853-864, 1985. IMPAIRED RELAXATION and diastolic filling of the left ventricle contribute importantly to the spectrum of symptoms experienced by patients with hypertrophic cardiomyopathy. Several studies of hypertrophic cardiomyopathy indicate that verapamil, administered intravenously or orally, improves indexes of left ventricular relaxation and diastolic filling.`X Verapamil also reduces symptoms and increases exercise tolerance in many patients with this disease.-H owever, the relationship between enhanced left ventricular diastolic filling resulting from verapamil and improved exercise tolerance has not been demonstrated conclusively.

show abstract

Section: Discussionmentioning

confidence: 99%

Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects.

et al. 1985

View full text Add to dashboard Cite

show abstract

“…'1 Easily discernible alterations in left ventricular relaxation indexes have been observed in patients with left ventricular hypertrophy (LVH) (despite normal systolic performance) and it has been suggested that slow, delayed, or prolonged relaxation might be an early marker of left ventricular disease. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] Much of the published work in this area incorporates measurement of endocardial length (or volume) transients that reflect filling properties of the left ventricular chamber, not necessarily the lengthening properties of an average (i.e., midwall) unit of myocardium. In this report, chamber filling and midwall fiber lengthening will be assessed in normal and hypertrophic hearts and attempts will be made to refine the conventional method of determining midwall length transients.…”

mentioning

confidence: 81%

Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.

Shimizu¹,

Zile²,

Blaustein³

et al. 1985

Circulation

147

View full text Add to dashboard Cite

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic hearts and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +-0.7 vs 3.1 0.8 sec (p < .02) at the endocardium, 2.3 -+ 0.4 vs 1.6 + 0.4 sec '(p < .02) at the midwall (conventional method), and 2.1 ± 0.3 vs 1.4 + 0.3 sec -' (p < .01 ) at the midwall (modified method). Chamber filling and fiber lengthening rates are depressed in patients with concentric LVH. Conventional measurements overestimate "true" fiber velocities more in those with LVH than in normal subjects; thus, the modified midwall method offers a theoretical advantage, especially in studies in which data from normal and hypertrophic hearts are compared. Circulation 71, No. 2, 266-272, 1985. INCREASED chamber stiffness in patients with left ventricular pressure overload hypertrophy has been largely attributed to increased myocardial mass; however, it is generally accepted that increased intrinsic myocardial stiffness and/or abnormal myocardial re-

show abstract

“…LV diastolic dysfunction -namely impaired myocardial relaxation and increased stiffness -is the hallmark of HFpEF [34][35][36][37][38][39][40][41], however, it is not the only underlying abnormality. Other factors -both cardiac and extracardiac -including increased arterial stiffness, altered ventricular-arterial coupling [42,43], endothelial dysfunction, reduced vasodilator reserve [44,45] and chronotropic incompetence [46,47] have been recently implicated in the pathophysiology of this complex syndrome.…”

Section: Pathophysiologymentioning

confidence: 99%

Heart Failure with Preserved Ejection Fraction

Čulić

2017

N Engl J Med

View full text Add to dashboard Cite

Heart failure with preserved ejection fraction (HFpEF) has recently emerged as a major cause of cardiovascular morbidity and mortality. Contrary to initial beliefs, HFpEF is now known to be as common as heart failure with reduced ejection fraction (HFrEF) and carries an unacceptably high mortality rate. With a prevalence that has been steadily rising over the past two decades, it is very likely that HFpEF will represent the dominant heart failure phenotype over the coming few years. The scarcity of trials in this semi-discrete form of heart failure and lack of unified enrolment criteria in the studies conducted to date might have contributed to the current absence of specific therapies. Understanding the epidemiological, pathophysiological and molecular differences (and similarities) between these two forms of heart failure is cornerstone to the development of targeted therapies. Carefully designed studies that adhere to unified diagnostic criteria with the recruitment of appropriate controls and adoption of practical end-points are urgently needed to help identify effective treatment strategies.

show abstract

Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study

Cited by 380 publications

References 16 publications

Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects.

Verapamil-induced improvement in left ventricular diastolic filling and increased exercise tolerance in patients with hypertrophic cardiomyopathy: short- and long-term effects.

Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.

Heart Failure with Preserved Ejection Fraction

Contact Info

Product

Resources

About