ABSTRACT
Cardiac amyloidosis may result in an aggressive form of heart failure (HF). Cardiac contractility modulation (CCM) has been shown to be a concrete therapeutic option in patients with symptomatic HF, but there is no evidence of its application in patients with cardiac amyloidosis. We present the case of TTR amyloidosis, where CCM therapy proved to be effective. The patient had a history of multiple HF hospitalizations due to an established diagnosis of wild type TTR-Amyloidosis with significant cardiac involvement. Since he was highly symptomatic, except during continuous dobutamine and diuretic infusion, it was opted to pursue CCM therapy device implantation. At follow up, a significant improvement in clinical status was reported with an increase of EF, functional status (6 min walk test improved from zero meters at baseline, to 270 m at 1 month and to 460 m at 12 months), and a reduction in pulmonary pressures. One year after device implantation, no other HF hospital admission was needed. CCM therapy may be effective in this difficult clinical setting. The AMY-CCM Registry, which has just begun, will evaluate the efficacy of CCM in patients with HF and diagnosed TTR amyloidosis to bring new evidence on its potential impact as a therapeutic option.
ABSTRACT
AIM: The purpose of this study is to assess the ability of resting echocardiography to detect an acute coronary syndrome (ACS) before the occurrence of ischemic electrocardiogram (ECG) changes or troponin-T elevations. METHODS: Four hundred and three patients who presented to the emergency room (ER) with chest pain, normal ECGs, and normal troponin-T levels were admitted to the cardiologist-run Chest Pain Unit (CPU) for further monitoring. They underwent serial resting echocardiography for monitoring of left ventricle wall motion (LVWM), ECG telemetry monitoring, and serial troponin-T measurements. RESULTS: An ACS was detected in 49 patients (12.1%). These 49 patients were then subdivided into three different groups based on the initial mode of detection of their ACS. In group A, 16 of 49 (32.6%) patients had ACS shown by echocardiographic detection of LVWM abnormalities. In group B, 24 of 49 (48.9%) patients had an ACS detected by ischemic ECG changes. In group C, 9 of 49 (18.3%) patients had an ACS detected by troponin-T elevations. The shortest time interval between CPU-admission and ACS-detection occurred in group A (A vs. B, P < 0.003; A vs. C, P < 0.0001). In group A, cardiac angiogram showed that the culprit coronary lesion was more frequent in the circumflex artery (11 out of 16; 68.7%) (LCx vs. LAD, P < 0.02; LCx vs. RCA, P < 0.001) and of these 11 patients with circumflex lesions, the ECG was normal in eight (72.7%) patients. CONCLUSION: This study demonstrates the utility of LVWM monitoring by serial echocardiography as part of a diagnostic protocol that can be implemented in a CPU. Furthermore, echocardiography could become an essential tool used in the diagnosis of ACS secondary to circumflex lesions.
