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[Left ventricular relaxation in myocardial diseases. Hemodynamic study]
Insights
Primary hypertrophic cardiomyopathy shows impaired left ventricular relaxation, while dilated cardiomyopathy may have secondary relaxation changes due to reduced contractility. These findings suggest distinct mechanisms in these heart conditions.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Biomedical Engineering
Context:
- Left ventricular relaxation is crucial for diastolic function.
- Primary hypertrophic cardiomyopathy (HCM) and dilated cardiomyopathy (DCM) are distinct heart muscle diseases.
- Accurate assessment of diastolic function is vital for diagnosis and management.
Purpose:
- To investigate and differentiate left ventricular relaxation patterns in HCM and DCM.
- To establish a simplified protocol for measuring ventricular relaxation using pressure and its first derivative.
- To explore the relationship between relaxation abnormalities and contractility in these cardiomyopathies.
Summary:
- A simplified protocol using left ventricular pressure and its first derivative (dp/dt) was developed to assess isovolumic relaxation time and rate.
- Patients with primary HCM exhibited prolonged relaxation duration and reduced relaxation rates (dp/dt min, dp/dt min/28P).
- In DCM, relaxation abnormalities appeared secondary to decreased contractility, unlike the primary relaxation deficits observed in HCM.
Impact:
- Findings support the hypothesis that relaxation changes are specific to hypertrophic cardiomyopathy.
- Contractility changes may be specific to dilated cardiomyopathy.
- This research aids in differentiating between HCM and DCM, potentially guiding therapeutic strategies.
Abstract:
Left ventricular relaxation as opposed to contraction, was studied by recordings of left ventricular pressure and its first derivation in primary hypertrophic cardiomyopathy without obstruction (25 cases, Group II) in primary dilated cardiomyopathy (33 cases, Group III) and in normal subjects (22 cases, Group I). Simultaneous recording of the pressure, the first derivation and intraventricular and intraaortic phonocardiogrammes showed the significance of certain features of the tracings and allowed a simplified protocol: ventricular relaxation was then defined from the pressure tracing (high fidelity recording) and its first derivation. The onset of isovolumic relaxation corresponded to the point of inflection on the descending part of the first derivation tracing, preceding its negative peak by an average of 0.02 s. The end of isovolumic relaxation corresponded to the crossing point of the atrial and ventricular pressure curves. In the absence of atrial pressure tracings the initial part of the rapid filling phase was included as far as the return of the first derivation tracing to its baseline (early diastole on the ventricular pressure tracing) as the duration of this period seemed remarkably constant (0.07 s). The parameters studied were: duration of isovolumic relaxation or the period defined above including the rapid filling phase; the average rate of fall of left ventricular pressure during this part of diastole; the value of the negative peak of the first derivation (dp/dt min); the rate of lengthening of the contractile elements at minimum dp/dt (dp/dt min/28P). Changes in relaxation were obvious in the pathological groups. The duration was increased and its average speed, dp/dt min, and dp/dt min/28 P were reduced. In the hypertrophic group, however, these changes seemed to be primary and contractility was usually unaffected. In dilated cardiomyopathy these changes could be considered secondary to decreased contractility. The hypothesis that changes in relaxation are specific for hypertrophic forms, and that changes in contractility are specific for dilated forms of primary cardiomyopathy may therefore be proposed.