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Ischemia and left ventricular dysfunction: a reciprocal relation?
D J van Veldhuisen1, A F van den Heuvel, P K Blanksma
1Department of Cardiology/Thoraxcenter, University Hospital Groningen, The Netherlands.
Insights
Congestive heart failure (CHF) impairs myocardial blood flow reserve, a condition that worsens with CHF severity. This study suggests ischemia may play a role in CHF development, particularly in dilated cardiomyopathy.
Area of Science:
- Cardiology
- Nuclear Medicine
- Physiology
Background:
- Myocardial ischemia can cause left ventricular (LV) dysfunction and congestive heart failure (CHF).
- The potential for CHF to cause myocardial ischemia is less understood.
- Assessing myocardial blood flow and metabolism is crucial for understanding heart function.
Purpose of the Study:
- To investigate whether congestive heart failure (CHF) impairs myocardial blood flow reserve.
- To explore the relationship between CHF severity and impaired blood flow reserve.
- To examine the presence of perfusion-metabolism mismatch in CHF patients.
Main Methods:
- Positron emission tomography (PET) with [13N]ammonia was used to measure myocardial blood flow (MBF) and flow reserve.
- Two patient groups were studied: idiopathic dilated cardiomyopathy and coronary artery disease (CAD) with varying LV function.
- Myocardial glucose metabolism was assessed using [18F]fluorodeoxyglucose (18FDG) uptake.
Main Results:
- Patients with idiopathic dilated cardiomyopathy showed impaired myocardial blood flow reserve compared to healthy controls.
- CHF patients with CAD also exhibited reduced myocardial blood flow reserve compared to those with normal LV function.
- A significant correlation was found between the degree of blood flow reserve impairment and CHF severity.
- A perfusion-metabolism mismatch was observed in a substantial portion of the myocardium in patients with dilated cardiomyopathy and CHF.
Conclusions:
- Myocardial blood flow reserve is significantly impaired in patients with congestive heart failure.
- The impairment of blood flow reserve is directly proportional to the severity of CHF.
- Findings suggest a potential pathogenetic role for myocardial ischemia in CHF, especially in dilated cardiomyopathy.
Abstract:
There is convincing evidence that (prolonged) episodes of myocardial ischemia lead to impairment of left ventricular (LV) function and ultimately to chronic congestive heart failure (CHF), but whether the opposite is also true has not been well established. We studied this issue in two groups of CHF patients with positron emission tomography (PET) by using [13N]ammonia (13NH3) as a tracer. In the first protocol we compared 12 patients with idiopathic dilated cardiomyopathy (who have normal coronary arteries) with 12 healthy controls. In the second protocol we studied a group of 24 patients with documented coronary artery disease (CAD). In this protocol, we compared patients with normal LV function to those with LV dysfunction and CHF. In patients with cardiomyopathy, myocardial blood flow at rest was normal but flow reserve (after dipyridamole infusion) was significantly impaired (1.7 +/- 0.08) compared with normal subjects (2.7 +/- 0.04; p <0.05). Furthermore, by examining [18F]fluorodeoxyglucose (18FDG) uptake, a perfusion-metabolism mismatch was observed in 24 +/- 6% of the myocardium in patients with cardiomyopathy as opposed to 0% of normals (p <0.05). In patients with CAD, myocardial blood flow reserve (measured in non-stenotic arteries to non-infarcted area) was impaired in CHF patients (1.7 +/- 0.06) compared to those with normal LV function (2.3 +/- 0.05; p <0.05). In both groups of CHF patients, the impairment of blood flow reserve showed a significant correlation with the severity of CHF. In conclusion, myocardial blood flow reserve is impaired in patients with CHF in proportion to the degree of CHF. Metabolic studies with 18FDG further show that, in patients with idiopathic dilated cardiomyopathy and CHF, flow-metabolism mismatch is present in a substantial part of the myocardium, suggesting a pathogenetic role for ischemia.