Slow heart rate recovery (HRR) predicts all-cause mortality. This study investigated the relationship between silent myocardial ischemia (SMI) and HRR in type 2 diabetes.The study enrolled 87 consecutive patients with type 2 diabetes and no chest symptoms. They underwent treadmill exercise testing and single-photon emission computed tomography imaging with thallium scintigraphy. Patients with abnormal myocardial perfusion images also underwent coronary angiography.SMI was diagnosed in 41 patients (47%). The SMI group showed slower HRR than the non-SMI group (18 ± 6 vs. 30 ± 12 bpm; P < 0.0001). HRR was significantly associated with SMI (odds ratio 0.83 [95% CI 0.75-0.92]; P = 0.0006), even after adjustment for maximal exercise workload, resting heart rate, maximum heart rate, rate pressure product, HbA(1c), use of sulfonamides, and a history of cardiovascular disease.HRR can predict SMI in patients with type 2 diabetes.
A healthy 73-year-old woman unpredictably developed Takotsubo cardiomyopathy syndrome (TTS) during Holter-electrocardiogram (ECG) recording. Thus, the complete chronological ECG data on the actual onset day of TTS were obtained. Many heart rate variability (HRV) parameters, including the low-frequency components (LF) and the high-frequency components (HF), on the actual onset day and in the healing phase were calculated. The interesting facts on the actual onset day were that the suppression of both LF and HF appeared earlier than the changes of the ECG waveform; and the LF/HF ratio remained within the normal range, although both LF and HF were markedly suppressed. The abnormality on the actual onset day was clear compared with the healing phase. It is noteworthy to obtain the chronological ECG data on the actual onset day of TTS in a healthy patient. The present data are unique in terms of being analyzed on the actual onset day. Although the HRV parameters, including LF and HF, were obviously abnormal, there is some skepticism about using HRV parameters as indices of cardiac autonomic activity. In the present case, it was concluded that the abnormality of cardiac autonomic activity contributed to the onset of TTS. These data are unlikely to ever be replicated, and we hope that this report helps elucidate the TTS mechanism.
When performing intravascular ultrasound studies, the backward echo image can show marked attenuation, although there are no calcified deposits and it may be impossible to detect the intraplaque architecture. The pathology underlying this phenomenon was investigated in autopsy specimens. We hypothesize that the mechanism responsible for the attenuation involves micro‐calcification and lipid in unstable plaques causing ultrasonic wave reflection and dispersion.
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