Physiologic mechanisms governing hemodynamic responses to positive inotropic therapy in patients with dilated cardiomyopathy.

AimsSome authors have hypothesized that left ventricular chamber dilatation in ischaemic and idiopathic cardiomyopathies results in spherical transformation. Aiming to characterize how this transformation occurs, a study was performed by comparing normal and dilated specimens regarding sphericity and proportionality in left heart chambers. It is important to provide data for the development of therapeutic strategies in these diseases.Methods and resultsAn anatomical study was performed by comparing normal (n = 10), ischaemic (n = 15), and idiopathic (n = 18) dilated human cardiomyopathic specimens regarding left ventricular chambers and their segmental proportionality to normal hearts. It was performed by capturing and processing images with proper software in three different levels of left ventricular chamber (basal, equatorial, and apical). These obtained data were analysed based on sphericity and proportionality by two dedicated indexes. Spherical shape: Calculated segmental indexes showed that dilated specimens were not spherical because they were smaller than as expected for a spherical shape (all values were <70% of a perfect sphere). Proportionality: There was no difference between basal index perimeters among groups, but apical index was lower in dilated specimens than in normal hearts, and so dilatation was not proportional to normal hearts.ConclusionsLeft ventricular chambers of anatomical specimens with dilated cardiomyopathies did not display a spherical shape and were not proportional to normal hearts.

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“…Thus, surgical and medical therapies can be tailored and targeted against each one of these components 13, 14, 15, 16, 24, 25…”

Section: Discussionmentioning

confidence: 99%

Left ventricular chamber geometry in cardiomyopathies: insights from a computerized anatomical study

et al. 2018

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“…LV shape was assessed by computation of end-diastolic and end-systolic sphericity indexes, ie, the ratio of the major to the minor axis at end diastole and end systole. 20 The size of the mitral annulus and the distance separating the plane of the mitral annulus plane from the coaptation between the mitral leaflets at end systole was also measured. 21 The presence and magnitude of MR were assessed by use of the regurgitant color jet over left atrium area method.…”

Section: Gas Exchange Analysismentioning

confidence: 99%

Contribution of Exercise-Induced Mitral Regurgitation to Exercise Stroke Volume and Exercise Capacity in Patients With Left Ventricular Systolic Dysfunction

et al. 2002

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Background-Functional mitral regurgitation (MR) is common in patients with heart failure and left ventricular (LV) dysfunction, and its severity may vary over time, depending primarily on the loading conditions. Because dynamic changes in the severity of functional MR may affect forward stroke volume, we hypothesized that exercise-induced changes in MR severity influence the stroke volume response of patients with LV dysfunction to exercise, and hence their exercise capacity. Methods and Results-Heart failure patients (nϭ25; mean age 53Ϯ12 years) with LV dysfunction underwent dynamic bicycle exercise at steady-state levels of 30%, 60%, and 90% of predetermined peak V O 2 . During each exercise level, right heart pressures, cardiac output, V O 2 , and MR severity were measured simultaneously. During exercise, MR severity, as evaluated by the ratio of MR jet over left atrium area, increased from 15Ϯ8% to 33Ϯ15%. Peak V O 2 , exercise-induced changes in stroke volume, and those in capillary wedge pressure correlated with the changes in MR (rϭϪ0.55, Ϫ0.87, and 0.62, respectively, PϽ0.01). The changes in MR severity also correlated with those in end-diastolic (rϭϪ0.75, PϽ0.01) and end-systolic (rϭϪ0.72, PϽ0.01) sphericity indexes and those in the coaptation distance (rϭ0.86, PϽ0.01). Conclusions-Our data indicate that in patients with LV dysfunction, exercise-induced changes in MR severity limit the stroke volume adaptation during exercise and therefore contribute to limitation of exercise capacity.

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“…The SOLVD investigators, in a placebo-controlled trial of symptomatic heart failure patients, also demonstrated a survival benefit with enalapril treatment of 16% risk reduction, although approximately one third of patients in the active treatment arm had stopped enalapril by the end of the study.21 Importantly, these investigators demonstrated a parallel benefit on frequency of hospitalization for worsening heart failure and a survival benefit largely attributable to a reduction in progressive heart failure in patients with low ejection fractions. Approximately 1 year later, the SOLVD investigators reported on the prevention arm of their study, which examined in a placebo-controlled fashion the effects of enalapril on patients with functional class I or II heart failure and left ventricular ejection fractions of 535% who were not receiving drug treatment for heart failure.75 Although no significant reduction in mortality was seen over the average follow-up of 37 months, there was a 20% reduction in hospitalization for new or worsening heart failure in enalapril-treated patients that was most pronounced among patients with the lowest ejection fractions. An unexpected and interesting finding from the SOLVD study was that on composite analysis of both treatment and prevention arms, enalapril reduced the frequency of both myocardial infarction (23%) and unstable angina (20%).…”

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confidence: 99%

Medical advances in the treatment of congestive heart failure.

Armstrong

Moe

1993

Circulation

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The increased incidence and prevalence of congestive heart failure place a high priority on novel treatment strategies. Left ventricular ejection fraction remains the single most valuable measurement providing both diagnostic and prognostic insights. The most systematic approach to heart failure involves an objective assessment of functional disability, to include exercise tests such as a 6-minute walk under standardized conditions. Left ventricular dysfunction incites a host of neurohumoral compensations that are of fundamental importance in the heart failure syndrome expression. Both vasoconstrictor and vasodilator neurohormones are stimulated and provide new therapeutic opportunities. The therapeutic approach to heart failure begins with a strong emphasis on prevention, patient education, and self-participation in therapy with respect to both its monitoring and adjustment. Diuretics remain a mainstay of therapy but, in the face of severe heart failure, may become ineffectual, requiring constant infusion of loop-active diuretics, combination diuretics, or diuretics in association with concomitant low-dose dopamine infusion. Vasodilator therapy has been an important advance: combination hydralazine and nitrate therapy was initially shown to be efficacious in improving survival, and more recently, angiotensin-converting enzyme (ACE) inhibitors, in the form of enalapril, have shown incremental benefit on survival over this combination. Interestingly, there is now evidence from both SOLVD and SAVE to demonstrate an unexpected and, as yet, unexplained reduction in the frequency of both unstable angina and myocardial infarction. Although, on balance, the weight of evidence concerning the long-term efficacy of inotropic agents has been disappointing, especially as it relates to their unfavorable effects on survival, recent information on vesnarinone, an agent with a complex and diversified mechanism of action, suggests that with appropriate doses, improved symptoms and survival are possible. A substantial amount of new information from randomized placebo-controlled trials attests to the symptomatic relief, hemodynamic improvement, and gain in exercise performance achieved by digoxin. A long-term survival study is ongoing to assess its effects on mortality. j3-Blockers, especially metoprolol, appear beneficial in some patients with heart failure, possibly related to their reduction in sympathetic nervous activity and restoration of J3-receptor population, with resultant improved contractile performance, enhanced myocardial relaxation, and overall increase in cardiac efficiency. Based on available evidence, the best contemporary approach to treatment involves the use of ACE inhibitors coupled with diuretic therapy, either continuous or intermittent, to relieve central or peripheral congestion. The addition of digoxin or a hydralazine nitrate combination is a logical next step, with commencement of low-dose 13-blocker a reasonable option. The residual mortality in the treatment groups of large-scale, contemporary, rando...

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Physiologic mechanisms governing hemodynamic responses to positive inotropic therapy in patients with dilated cardiomyopathy.

Cited by 126 publications

References 50 publications

Left ventricular chamber geometry in cardiomyopathies: insights from a computerized anatomical study

Left ventricular chamber geometry in cardiomyopathies: insights from a computerized anatomical study

Contribution of Exercise-Induced Mitral Regurgitation to Exercise Stroke Volume and Exercise Capacity in Patients With Left Ventricular Systolic Dysfunction

Medical advances in the treatment of congestive heart failure.

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