Fleckenstein's hypothesis revisited: excessive myocardial calcification after prolonged high dose catecholamine treatment: a case report

Abstract

Background: Myocardial calcification after prolonged highly dosed catecholamine treatment has been described experimentally. Here, we demonstrate myocardial calcifications by high-dose catecholamine treatment leading to chronic heart failure in patients.

Case summary: A 62-year-old Caucasian woman presented with central pulmonary embolism, developing acute heart failure, and cardiogenic shock. Twenty-six days of high-dose norepinephrine treatment had to be administered to maintain circulation. After 74 days of intensive care treatment, the patient fortunately recovered but was readmitted to emergency ward because of dyspnoea and congestion. Computed tomography pulmonary angiography ruled out recurrence of pulmonary embolism, but depicted massive intramural cardiac calcifications, which were not present before treatment. Coronary angiography showed normal coronary arteries, and myocardial biopsy excluded infectious myocarditis. There was no evidence for sarcoidosis, thyroid disease, tuberculosis, or hyperparathyroidism. Oral heart failure treatment was initiated and at the 7 week follow-up the patient remained symptomatic with New York Heart Association functional Class III, while right and left ventricular function had recovered.

Discussion: Prolonged activation of the heart by catecholamines leading to myocardial calcifications has first been examined experimentally by Fleckenstein et al. Herein, we are able to show, that this can occur in clinical situations. Careful dosing of catecholamines and early use of non-catecholamine-based haemodynamic support is recommended to avoid consecutive impairment of heart function and heart failure.

Keywords: Case report; Catecholamines; Congestive heart failure; Myocardial calcification; Myocardium.

Figure 1

Total doses of norepinephrine in mg/24 h (bars) and course of systolic and diastolic blood pressure (blue lines) and heart rate (red line) over time.

Figure 2

Initial contrast-enhanced computed tomography of the thorax (A) demonstrating a normal density of the left ventricular myocardium. At that time pulmonary embolism was demonstrated. On corresponding follow-up computed tomography scans 2 weeks (B) and 2 months later (C) the left ventricular myocardium depicts markedly hyperdense areas at the apex and the lateral wall suggestive of diffuse calcifications (arrowheads).

Figure 3

Cardiac magnetic resonance imaging (A and C) and computed tomography (B and D) acquired with ECG synchronization. On T2-weighted STIR images in three-chamber view (B) the left ventricular myocardium shows a normal signal intensity without signs of myocardial oedema. T1-weighted inversion-recovery sequences in short-axis orientation (C) after intravenous application of contrast show a marked late gadolinium enhancement of the anterior and anterolateral aspects of the left ventricular wall (arrowheads). B and C display corresponding multiplanar reconstructions in three-chamber view and short-axis orientation of the unenhanced cardiac computed tomography scan with ECG synchronization. Note again the markedly hyperdense depictions of the left ventricular wall corresponding to diffuse calcifications.

Figure 4

Histology in Masson Trichrome staining showing replacement of ventricular myocardium by calcificated components.