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Left ventricular function in chronic anemia: evidence of noncatecholamine positive inotropic factor in the serum
Insights
Anemia enhances cardiac contractility, independent of preload and afterload changes. This study found that anemia serum increased myocardial tension development, suggesting a direct positive inotropic effect in anemia.
Area of Science:
- Cardiology
- Hematology
- Physiology
Background:
- Enhanced left ventricular (LV) performance in anemia is known, but its cause, particularly regarding contractility, remains debated.
- Previous studies suggest preload and afterload alterations contribute, but a direct effect on myocardial contractility is controversial.
Purpose of the Study:
- To investigate whether chronic anemia increases left ventricular (LV) contractility.
- To determine if anemia-associated cardiac performance changes are due to intrinsic myocardial contractility enhancement.
Main Methods:
- Noninvasive LV function assessment using M-mode echocardiography and blood pressure in anemic patients and controls.
- In vitro assessment of cat papillary muscle tension development using serum from anemic patients and controls.
- In vitro assessment of tension development after beta-adrenergic blockade.
Main Results:
- Anemic patients showed increased stroke volume, fractional shortening, and rate of circumferential shortening.
- Anemia serum significantly increased maximal developed tension and maximal rate of tension development in isolated papillary muscles compared to control serum.
- These contractility enhancements persisted after beta-adrenergic blockade, indicating a non-beta-adrenergic mechanism.
Conclusions:
- Chronic anemia is associated with enhanced left ventricular (LV) contractility.
- Anemia serum possesses a direct positive inotropic effect on myocardial function, independent of beta-adrenergic pathways.
- This intrinsic contractility enhancement contributes to the altered cardiac performance observed in anemia.
Abstract:
The enhanced left ventricular (LV) performance observed in anemia has been attributed to changes in preload and afterload. Whether there is a concomitant increase in contractility is controversial. Seventeen patients with chronic anemia (hematocrit range 17 to 30%) and 17 control subjects, matched by age and sex, were studied. In 10 patients and 10 control subjects (group I), a noninvasive evaluation of LV function through M-mode echocardiography and cuff blood pressure recording was performed. In patients with anemia, stroke volume increased 43% (p less than 0.01), fractional shortening 21% (p less than 0.001), and mean rate of circumferential shortening 32% (p less than 0.001). In patients with anemia, end-systolic stress decrease 27% (p less than 0.05) and diastolic blood pressure 21% (p less than 0.001). The effect of serum from these patients and control subjects on the development of isometric tension by isolated cat papillary muscles was assessed compared with the basal (Ringer-Locke bath) values. Anemia serum increased maximal developed tension 21% and maximal rate of tension development 20% relative to basal levels. These changes were significantly higher (p less than 0.001) than the increases produced by control serum (8% and 7%, respectively). In the 7 patients with anemia in group II and their matched controls, the in vitro isometric tension characteristics were assessed before and after blocking beta adrenoreceptors with propranolol, 10(-6) M. The observed increase in the developed tension persisted after beta blockade, as well as the enhancement of the maximal rate of tension development. Plasma catecholamine levels in this group II were within the normal range.(ABSTRACT TRUNCATED AT 250 WORDS)