Docetaxel, a taxoid chemotherapy agent, may induce fluid retention. We present a case of metastatic breast cancer in which high output caused by docetaxel-induced fluid retention resulted in heart failure due to left ventricular outflow tract (LVOT) obstruction. A 58-year-old woman presented with exertional dyspnea and anasarca. The jugular venous pressure was elevated, and the carotid pulse was pulsus bisferiens with a spike-and-dome configuration. On auscultation, a mid-late systolic murmur that did not radiate to the neck but increased with the Valsalva maneuver was noted. Echocardiography revealed a left ventricular ejection fraction of 63% with systolic anterior motion (SAM) of the mitral valve, resulting in LVOT obstruction with a resting pressure gradient of 64 mmHg and moderate to severe mitral regurgitation. Treatment with carvedilol, trichlormethiazide, and an increased dose of furosemide gradually improved her symptoms, physical findings, and echocardiographic abnormalities. This case highlights the importance of recognizing high-output heart failure along with LVOT obstruction in patients scheduled to receive docetaxel.

To clarify the genesis of the aortic thudding sound (AK), phono-, mechano- and pulsed Doppler echocardiography were performed in 16 patients with pure aortic insufficiency (AI), 3 with AI associated with mild aortic stenosis (AIs) and 5 with AI associated with mitral insufficiency (AI + MI). The results obtained were as follows: 1) AK was composed of two components, that is, one (AK1) occurred in early systole and the other (AK2) near the end point of an ejection systolic murmur. Patients studied were divided into 4 groups following the appearance of AK1 and/or AK2: group with only AK1 (4 cases), group with only AK2 (7 cases), group with both AK1 and AK2 (5 cases) and group without AK (8 cases). 2) AK1 was a low frequency sound and was well recorded from the cardiac base to the right supraclavicular region. AK1 was not observed in cases with mild to moderate AI and with AI associated with mild AS. In atrial fibrillation, when the preceding R-R intervals were long, AK1 was loud and appeared in early systole, and when short, small and in mid-systole. Marked augmentation of AK1 was observed in the first beat after premature ventricular contraction with a compensatory pause. 3) AK2 was also low in frequency and was most intensively recorded near the apex. Although the intensity of AK2 tended to increase in the severe cases of AI, AK2 could be observed in mild to moderate cases. Intensity of AK2 also showed the post-extrasystolic potentiation similar to that of AK1. 4) The carotid pulse showed pulsus bisferiens in all cases with AK2 (group with only AK2 and group with both AK1 and AK2). On the other hand, in cases without AK2 (group without AK and group with only AK1), carotid pulse showed a monophasic systolic wave except 3 cases. These results suggested that there was a close relationship between AK2 and pulsus bisferiens in the carotid pulse. (5) In the apex cardiogram (ACG), systolic notches coincident with AK1 and/or AK2 were observed in 10 of 12 cases with AK2 and in 4 of 9 cases with AK1. In cases without AK, however, no notch was seen in ACG. Therefore, these notches might be resulted from the shock of the anterior chest wall produced simultaneously with the occurrence of AK. 6) Flow patterns at the left ventricular outflow tract (aortic flow patterns) were recorded in 13 cases, including 3 with only AK1, 2 with only AK2, 3 with both AK1 and AK2 and 5 without AK. In 5 of 13 cases the flow patterns were recorded simultaneously with phonocardiograms. Systolic aortic flow showed biphasic patterns in all cases with AK2, and monophasic patterns in cases without AK2. AK1 occurred coincidentally with the first peak of the biphasic flow patterns, and AK2 with the second peak. These results suggested that AK1 might be produced by rapid ejection of massive amount of blood containing a regurgitant flow into the aorta with the ordinarily distensiblwe aortic wall, and AK2 by the clash between the second ejected flow and the reflected flow returning from the peripheral artery against the first ejected flow.

The volume overload type of heart often observed in endurance athletes, was simulate a diseased heart. We used a battery of noninvasive graphic techniques, i.e., echocardiogram, apexcardiogram, carotid pulse, electrocardiogram, vectorcardiogram, phonocardiogram, systolic time intervals, and treadmill stress testing in 12 professional marathon runners, mean age 33.8 +/- 11.1. Twenty nonathletes matched for age, height, sex, and weight served as a control group. Left ventricular (LV) end-diastolic dimension in marathon runners averaged 5.53 +/- 0.5 cm compared to 4.81 +/- 0.04 cm in nonathletes (p less than 0.001), LV end-diastolic volume was 172.69 +/- 43.3 ml compared to 113.57 +/- 30.41 ml in nonathletes (p less than 0.001), stroke volume was 122.27 +/- 32.8 ml compared to 78.42 +/- 20.44 ml in non-athletes (p less than 0.001), the thickness of the posterior LV wall was 1.0 +/- 0.2 cm compared to 0.7 +/- 0.1 cm in nonathletes (p less than 0.001), and LV mass was significantly increased, 212.43 +/- 55.8 g compared to 123.48 +/- 24.54 g in non-athletes (p less than 0.01). Left atrium and aortic root were also relatively larger in athletes (p less than 0.01). Right ventricular end-diastolic dimension was enlarged in marathon runners (2.02 +/- 0.65 cm). No statistically significant differences were noted in ejection fraction, percentage of internal diameter shortening (% delta D) and PEP/LVET. The carotid tracing had a bisferiens pulse in five marathon runners. The apexcardiogram showed a bifid systolic thrust in three and absence of abnormal A wave. These abnormalities were related to the overload type of heart as proven by echocardiogram. "Early repolarization syndrome" (abnormal RS-T segment elevation) and notched T waves in ECG had a counterpart a semilunar configuration in the VCG. Three athletes met ECG criteria and one met VCG criteria of LVH. The treadmill exercise ECG was negative in all 12 athletes. Biventricular enlargement and increased left ventricular mass are present in the marathon runner's heart. Myocardial contractility at rest was, however, not statistically different from nonathletes.