Key result
Among 162 HCM patients followed for 13.3 years, 16 developed distinct left ventricular wall motion abnormalities (11 with apical segmental dysfunction and 5 with generalized hypokinesis).
Why the study?
What are the clinical features and mechanisms of gradual development of left ventricular wall motion abnormalities in patients with hypertrophic cardiomyopathy?
Cohort (n=162)
What are the clinical features and mechanisms of gradual development of left ventricular wall motion abnormalities in patients with hypertrophic cardiomyopathy?
Patients with hypertrophic cardiomyopathy can develop two distinct types of left ventricular wall motion abnormalities (apical segmental dysfunction vs. generalized hypokinesis) that have different initial manifestations and clinical courses.
LV wall motion abnormalities may emerge during HCM follow-up, warranting surveillance; leaves open mechanisms, prognosis, and interventions.
During the long-term follow-up of patients with hypertrophic cardiomyopathy (HCM), some patients develop left ventricular (LV) wall motion abnormalities in the absence of fixed coronary artery disease. The purpose of this study is to clarify which clinical features in patients with HCM seem to influence gradual development of LV wall motion abnormalities over an extended period of time. The study investigates the incidence, mechanism and predictors of these abnormalities. In this retrospective study of 162 patients with HCM, followed-up for an average of 13.3 years, we focused our attention on 16 patients who gradually developed two different forms of LV wall motion abnormality. In 11 of these 16 patients, apical segmental dysfunction with midzone obstruction was recognized; the remaining five patients showed generalized hypokinesis, as seen in dilated cardiomyopathy. The 11 patients with apical segmental dysfunction presented with extensive apical hypertrophy reaching the midventricular level at first examination. The five patients with generalized hypokinesis showed a slight decrease in LV contractility and reduced localized antero-apical wall motion even at initial examination. None of the patients in either group developed the other group's features during their clinical course. These two groups had different initial manifestations and pursued different clinical courses, suggesting that the underlying mechanisms causing wall motion abnormalities are different.
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Ishiwata et al. (1993) conducted a cohort in Hypertrophic cardiomyopathy (n=162). Among 162 HCM patients followed for 13.3 years, 16 developed distinct left ventricular wall motion abnormalities (11 with apical segmental dysfunction and 5 with generalized hypokinesis).
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