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[Hemorrheological changes in ischemic heart disease]
Insights
Patients with ischemic cardiopathy exhibit significant hemorheological changes, including increased blood viscosity and reduced red blood cell deformability, particularly during acute myocardial ischemia. Localized hemorheological abnormalities in the myocardium suggest a syndrome dependent on tissue ischemia.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Biophysics
Context:
- Ischemic cardiopathy presents unique hemorheological characteristics.
- Previous studies indicate modifications in rheological parameters in patients with heart disease.
- Hemorheological changes are more pronounced in acute myocardial ischemia.
Purpose:
- To investigate hemorheological alterations in ischemic cardiopathy.
- To compare hemorheological parameters in systemic venous blood versus coronary sinus blood.
- To assess the impact of atrial pacing on myocardial hemorheology.
Summary:
- Patients with ischemic cardiopathy show statistically significant increases in blood and plasma viscosity and decreased red blood cell deformability compared to healthy subjects.
- Acute ischemic events, like angina and myocardial infarction, exacerbate these hemorheological changes.
- Coronary sinus blood reveals worse viscosity and red cell filtrability than systemic venous blood, with atrial pacing inducing significant hemorheological deterioration in positive pacing subjects, indicating local myocardial hyperviscosity linked to ischemia.
Impact:
- Findings suggest a localized hyperviscosity syndrome in the myocardium, directly related to tissue ischemia.
- This research deepens the understanding of the pathophysiology of ischemic heart disease.
- Highlights the potential for hemorheological markers in diagnosing and managing ischemic cardiopathy.
Abstract:
Ischemic cardiopathy in its various clinical manifestations, whether acute (angina pectoris or myocardial infarction) or chronic (chronic coronary insufficiency), has shown in recent years particular hemorheological characteristics of its own. The observation of patients with such diseases has allowed us to record the existence of modifications in the parameters indicative of rheological damage. Numerous studies have been made, many of which are still in progress, with the aim of clarifying the relationships between these data and the disease. In our experience an increase in blood and plasma viscosity and a decrease in red cell deformability are often present in a manner which is statistically significant, if these patients are compared with normal subjects. Hemorheological change is more evident in the acute forms of myocardial ischemia. In fact, in angina pectoris the occurrence of pain is always accompanied by an increase in blood viscosity and by a worsening of red cell deformability both during spontaneous crises and during provocative tests. The hemorheological damage tends to diminish fairly rapidly when the crisis is over, even if the level of stabilization proves to be still higher than normal. In myocardial infarction higher levels of viscosity appear for a brief period after the onset with a slight tendency to diminish up until the 30th day. With the aim of ascertaining whether the alteration is more evident precisely at the point where the ischemia occurs, we chose a necessarily limited number of subjects, undergoing coronarography and atrial pacing for diagnostic purposes, and decided to control the hemorheological data not only in the systemic venous blood but also in the blood taken from the coronary sinus. Our data has shown that the level of viscosity and of red cell filtrability, in the blood taken from the coronary sinus, is worse than those of the systemic venous blood and that, after atrial pacing, in negative pacing subjects the variations are of slight significance whilst in positive pacing subjects we observe a rapid increase in viscosity and a decrease in red cell filtrability. This seems to confirm what we have already observed in the limbs affected by peripheral ischemia, and to demonstrate the existence of a local hyperviscosity syndrome which, even in the myocardium, appears to be dependent on the tissue ischemia.