JOURNAL ARTICLE

[Hemodynamics and clinical data in chronic coronary disease with severe left ventricular systolic dysfunction]

P G Marinato, E Dametto, I Maragno, R Razzolini, P Chinellato, G Santostasi, S Dalla Volta
Cardiologia: Bollettino Della Società Italiana di Cardiologia 1996, 41 (4): 349-59
8674104
To elucidate how symptoms and signs of chronic heart failure are related to the filling pressure and cardiac output at rest, 58 patients (55 males, 3 females, mean age 57 +/- 9 years, range 30-75) with left ventricular ejection fraction (LVEF) < or = 30% and a lesion > or = 50% on a major coronary branch have been selected from patients submitted in 1985-1993 to a complete right and left cardiac catheterization including ventriculography and coronary angiography. Patients with recent myocardial infarction (MI), unstable angina, associated heart diseases or recent changes in body weight and in diuretic therapy were excluded. Clinical data were obtained at cardiac catheterization time from history, physical examination, chest X-ray and ECG. Patients with angina as limiting symptom were excluded from NYHA functional classification. Pulmonary venous congestion (PVC) was defined on X-ray as: absent, venous redistribution, interstitial pulmonary edema (IPE). Mean pulmonary capillary wedge pressure (PCWP) was recorded under fluoroscopy and cardiac index was measured by the Fick method. On the whole group, 96% of patients had had one or more MI (on ECG necrosis was anterior in 58%, inferior in 9%, anterior and inferior in 26%), 69% were in NYHA functional class III or IV, 54% had IPE and 45% had mitral regurgitation. 71% were under treatment with digitalis, 74% with diuretics and 39% with ACE-inhibitors. PCWP was correlated with LVEDV (r = 0.34; p < 0.001) but neither with LV mass nor with LV mass/volume ratio. It was significantly higher (p < 0.01) in patients with mild-moderate mitral regurgitation, in patients with necrosis involving both anterior and inferior walls (26 +/- 6 vs 21 +/- 8 mmHg in patients with single wall necrosis, p < 0.05) and in patients with multiple MI (26 +/- 7 vs 20 +/- 8 mmHg in patients with no or single MI, p < 0.02). Moreover, it was neither correlated with functional classification nor with PVC: of patients with PCWP > 24 mmHg, 14% were in II NYHA functional class and 21% had no PVC while of patients with PCWP < 15 mmHg, 36% were in NYHA functional class IV and 7% had IPE. Cardiac index was reduced below 2.3 l/min/m2 in 21% of patients: these patients had increased pulmonary (p < 0.0002) and systemic (p < 0.0001) vascular resistance, increased systolic (p < 0.001) and diastolic (p < 0.01) pulmonary artery pressure and reduced LVEF (p < 0.01) and right ventricular ejection fraction (p < 0.03). Furthermore, on the whole patients an inverse correlation was found between cardiac index and functional classification (r = -0.42; p < 0.01). The reliability of NYHA functional class IV, physical signs of heart failure and IPE for estimating PCWP > 24 mmHg and cardiac index < 2.3 l/min/m2 was rather limited although high specificity was shown for gallop sounds (92 and 97%) and jugular vein distension (88 and 97%). In conclusion, in coronary patients with chronic severe LV systolic dysfunction a mismatch between clinical data and central hemodynamics is not rare. The reliability of functional class, X-ray PVC and physical signs to predict central hemodynamics in fairly limited.

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