Intracardiac metastasis of a Malignant Mixed Mullerian tumor (MMMT): progressive dyspnoea due to obstruction of the left atrium and the left ventricle without left ventricular dysfunction or primary lung disease.

Malignant Mixed Mullerian tumors (MMMT) are rare gynecological tumors. Even with surgical treatment, chemotherapy, and/or radiotherapy, outcome is poor. MMMTs are known to metastasize to the liver, the abdomen, and the lungs. One case of an ocular metastasis has been reported. In a 61-year-old female patient who had undergone surgical resection of a Mullerian tumor of the uterus 26 months prior to being admitted to our department, we found an obstructing left atrial mass. Histopathologic assessment of this lesion after surgical resection revealed a Mullerian tumor metastasis. Immediately after surgery, the patient was asymptomatic, but was readmitted 4 months later with dyspnoea. Echocardiography and CT revealed new masses in the left atrium and left ventricle. On a literature review, we did not find any description of left atrial and left ventricular occluding metastases of MMMT.

Effects of different AT1-receptor antagonists in the therapy of severe heart failure pretreated with ACE inhibitors.

BACKGROUND: The efficacy of ACE-inhibitors and beta blockers is well documented in the therapy of heart failure. As pharmacological mechanisms of ATI-receptor-antagonists differ, an additional positive effect can be expected when combining these drugs. METHODS: Eighty patients (67.9 +/- 9.9 years) with severe chronic heart failure receiving long-term medication with diuretics, ACE-inhibitors and partially beta blockers (72.5%), were randomized after clinical recompensation to eprosartan (477.5 +/- 143.7 mg/d), telmisartan (65.9 +/- 17.7 mg), candesartan (11.9 +/- 4.0 mg) or no sartan, according to a prospective study. Haemodynamic measurements by impedance cardiography were performed (mean observation time 15.8 days). RESULTS: Additional sartan treatment resulted in an improvement of cardiac output from 2.32 +/- 0.69 to 3.12 +/- 1.24 l/min (P = 0.003) in the eprosartan group, from 2.24 +/- 0.59 to 2.76 +/- 0.91 l/min (P = 0.001) in the telmisartan group and from 2.76 +/- 0.84 to 3.11 +/- 0.94 l/min (P = 0.02) in the candesartan group. Furthermore, a significant decrease of the total peripheral resistance was measured under eprosartan (23%; P = 0.002), telmisartan (18%; P = 0.002) and candesartan treatment (11.5%; P = 0.049); in the subgroup of combined therapy with beta blockers, ACE-inhibitors and ATI-antagonists a significant increase in cardiac output was also observed. No change was observed in the control group without additional sartan treatment concerning cardiac output and resistance reduction. CONCLUSIONS: The additional treatment with different ATI-receptor-antagonists resulted in an increase of the cardiac output and a decrease of the peripheral resistance. This beneficial effect may be due to the additional property of sartans to block the interaction of locally and not-ACE-generated angiotensin II with their vascular and myocardial ATI-receptors.

Effects of AT1 receptor antagonist therapy in patients with severe heart failure pretreated with angiotensin-converting enzyme inhibitors.

BACKGROUND: The efficacy of angiotensin-converting enzyme (ACE) inhibitors is well documented in the treatment of chronic severe heart failure. Because pharmacological mechanisms of angiotensin II type 1 (AT1) receptor antagonists differ from the effects of ACE inhibitors, an additional positive effect can be expected by combining these drugs. METHODS: Sixty patients (mean age 68.3+/-10.0 years) with severe chronic heart failure receiving long term medication with digitalis, diuretics, ACE inhibitors and in part beta-blockers (68.3%) were randomly assigned after clinical recompensation to three groups: additional therapy with eprosartan (477.5+/-143.7 mg/day), telmisartan (65.9+/-17.7 mg/day) and control group according to a prospective study design. Hemodynamic measurements by impedance cardiography were performed before and during the observation period (9.6+/-3.4 days). RESULTS: Additional sartan treatment resulted in an improvement in cardiac output from 2.32+/-0.69 L/min to 3.12+/-1.24 L/min (P=0.003) in the eprosartan group and from 2.24+/-0.59 L/min to 2.76+/-0.91 L/min (P=0.001) in the telmisartan group; cardiac output in the control group did not increase. Furthermore, a significant decrease in total peripheral resistance was observed during treatment with eprosartan (23%, P=0.002) and telmisartan (18%, P=0.002). In the subgroup receiving combined therapy with beta-blockers, ACE inhibitors and AT1 antagonists, a significant increase in cardiac output was also observed. CONCLUSIONS: The additional treatment with AT1 receptor antagonists resulted in an increase in the cardiac output and a decrease in the peripheral resistance. This beneficial effect may be due to the additional property of sartans to block the interaction of locally and non-ACE-generated angiotensin II with their respective vascular and myocardial AT1 receptors.

Relation between N-terminal pro-brain natriuretic peptide values and invasively measured left ventricular hemodynamic indices.

BACKGROUND: Pro-brain natriuretic peptide (proBNP) is synthesized in the left ventricle. In response to transmural pressure, it is secreted into the circulation and consequently cleaved to yield the active hormone BNP and its N-terminal fragment (NT-proBNP). Determination of NT-proBNP is used as an aid in the diagnosis of left ventricular dysfunction. METHODS: We analyzed NT-proBNP-levels before left-heart catheterization in 115 patients. At the end of the study, we compared the NT-proBNP values to the invasively measured hemodynamic indices (left ventricular ejection fraction, maximum change in pressure over time [dP/dt(max)] and left ventricular end-diastolic pressure) and the clinically observed New York Heart Association (NYHA) classifications. RESULTS: A significant (P=0.008) increase of the NT-proBNP values was observed in cases of low ejection fraction (less than 41%). Furthermore, a significant (P=0.03) increase of the NT-proBNP values was measured in cases of heavily reduced dP/dt(max) (less than 1500 mmHg/s). The increase of NT-proBNP values in cases of high end-diastolic pressures was distinct but not significant. In the clinical observation (NYHA classification), a significant increase of NT-proBNP levels corresponded to increasing severity of heart failure. However, a large standard deviation was seen in all groups. CONCLUSION: Concerning low ejection fractions, a high end-diastolic pressure and strong reduced dP/dt(max) in all cases an increase of pro-BNP-values was seen. However, the partly reported strong correlation of the BNP value to the left ventricular ejection fraction, dP/dt(max) and left ventricular end-diastolic pressure results was not found in the cases of middle and moderate heart failure, in contrast to the clinical observation. Regarding the large standard deviation, it may be possible to discriminate an unfavourable course of heart failure in an early stage.