Author + information
- Received April 8, 1991
- Revision received August 19, 1991
- Accepted September 3, 1991
- Published online March 1, 1992.
- Takashi Nakamura, MD*,1,
- Kinya Matsubara, MD1,
- Keizo Furukawa, MD1,
- Akihiro Azuma, MD1,
- Hiroki Sugihara, MD1,
- Hiroshi Katsume, MD1 and
- Masao Nakagawa, MD1
- ↵*Address for reprints: Takashi Nakamura, MD, Second Department of Medicine, Kyoto Prefectural University of Medicine, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto 602, Japan.
In 20 of 198 patients with hypertrophic cardiomyopathy, Doppler color flow imaging revealed diastolic paradoxic jet flow across the obliterated left ventricular apex toward the base that suggested the presence of a discrete apical chamber. This prospective study characterized echocardiographic, ventriculographic and scintigraphic findings in these patients, as well as their clinical features.
Although echocardiography did not directly show the apical chamber in 13 of the 20 patients, left ventriculography always revealed a small apical outpouching separated from the major basal cavity. Systolic bulging of the apex was always followed by early diastolic shrinkage together with persistent cavity narrowing between the two chambers.
After the systolic jet flow, the paradoxic jet flow lasted for 366 ± 160 ms after aortic valve closure and always extended into the diastolic filling period. The maximal velocity of the paradoxic jet flow occurred during isovolumetric relaxation and the mean velocity was 2 ± 0.8 m/s, indicating a higher diastolic pressure in the apical chamber than in the main ventricle. Compared with patients who manifested cavity obliteration alone, patients with a paradoxic jet flow more often developed systemic embolism (p < 0.01), ventricular tachycardia (p < 0.05) and thallium perfusion abnormalities localized to the apical region (p < 0.01).
Thus, paradoxic jet flow could be an important marker of concealed apical asynergy and the risk of adverse clinical events. The higher diastolic apical pressure suggested by the flow may contribute to the development of an apical aneurysm, even in the absence of fixed coronary artery disease.
- Received April 8, 1991.
- Revision received August 19, 1991.
- Accepted September 3, 1991.
- American College of Cardiology Foundation