A 67-year-old male patient with a history of hypertension presented acute onset severe retrosternal chest pain and was diagnosed with extensive anterior myocardial infarction based on tombstone ST segment elevation in V1-V6 leads and remarkably increased cardiac troponin I. His physical examination revealed an accentuated pulmonary component of the second heart sound, tricuspid systolic murmur, and increased breath sound. An emergent coronary angiogram revealed occlusion in the left anterior descending coronary artery (LAD). After LAD revascularization, TTE was employed for cardiac morphology and function assessment, the left ventricular ejection fraction (LVEF) was 52%, and the left ventricular end diastolic diameter was 56 mm. He was discharged on dual anti-platelet therapy with aspirin and ticagrelor, as well as rosuvastatin, beta-blocker, and ACE inhibitor.
The patient did not follow the rehabilitation advices after discharge from our center. He often participated in high-intensity physical activity such like mountain climbing and long-distance running and experienced colds twice. Six months later, despite the complete revascularization of LAD and standard heart failure therapy, he started to experience progressive shortness of breath and fatigue because of the progression of HF, a New York Heart Associate Function class III–IV. He referred to our center again for further assessment and treatment, and the TTE revealed a notable reduction of LVEF (35%) and left ventricular enlargement (diastolic diameter, 66 mm). Moreover, the left aneurysm was developed, the estimated pulmonary artery pressure (PAP) was 30 mmHg, and the concentration of NT-proBNP increased to 1,424 pg/ml with normal renal function.
Considering the remarkable maladaptive LV remodeling and considerable LVEF reduction. The patient refused to undergo surgical ventricular reconstruction. To reconfigure the geometry of left ventricle and improve the cardiac function, he accepted to evaluate the possibility of parachute device implantation and received further computed tomography (CT) for proper device size selection (Fig. 1). The patient experienced multi-slice CT scan to check if he has left ventricular thrombus, pseuduchorda, or severe calcification, which could affect parachute deployment. Thereafter, left ventricular morphological parameter was measured by core laboratory. The quantitative assessment included diastolic and systolic assessment. Furthermore, maximum diameter shortening and diameter shortening based on mean diameter was carried out, and LV ejection was evaluated by CT. According to his left ventricular anatomy, we recommended the parachute device with a size of 85 mm and standard foot height.
Details of the device and procedure have been previously published[3, 7, 8]. In brief, the device includes a delivery system with a balloon that facilitates the expansion of the device and a pre-shaped delivery catheter and dilator. After the device is expanded, the occlusive membrane provides a barrier to seal off the static chamber on the distal side of the device (Figs. 1F and 1G). With parachute deployment, the patients received low-dose aspirin and anticoagulation with warfarin to prevent potential thrombosis. We performed TTE 4-day post-implantation, and his LVEF increased to 44%, the diastolic diameter decreased to 59 mm, and the estimated PAP decreased to 26 mmHg. His shortness of breath and fatigue was remarkably relieved, and NT-proBNP decreased to 771 pg/ml. The patient was discharged after his international normalized ratio (INR) became stable at 1.8–2.5, remained with statin, ACEI, and beta-blocker treatment.
However, in the next 19 months, the patient was hospitalized for six times because of heart failure progression. The patient did not follow our advice strictly, improper exercise enhanced the remodeling of the left ventricle. In addition to progressive HF, his blood pressure, LVEF met remarkable reduction. Besides, the diameter of LV, estimated pulmonary artery pressure, and NT-proBNP dramatically increased. In the terminal stage of his life, we also found a thrombus at the top of the parachute device. The patient has stopped warfarin treatment for 6 months at that time, and his INR was 1.25, which is insufficient to dissolve the thrombus. The regurgitation flow through the parachute (in the highlighted circle of Fig. 2D) indicate that the device has deviated from the original location.
We have conducted coronary angiography to exclude potential coronary vessel stenosis. The TTE revealed that his diastolic diameter of LV was remarkably elevated to 72 mm, the LVEF decreased to 32%, and the concentration of NT-proBNP exceeded 30,000 pg/ml (Table 1). The worsened condition of this patient was supported by the echocardiogram (Fig. 2). Before and right after the parachute implantation, even with dilated left ventricular chamber, only slight regurgitation was observed (Figs. 2A and 2B). The device was deployed to cover the aneurysm, it did not affect the function of papillary muscle. However, the continuous maladaptive remodeling enlarged the chamber of left ventricle, revealing a notable mitral regurgitation (Figs. 2C and 2D). The patient refused to accept ICD, CRT, and CRTD treatments. Ultimately, severe mitral regurgitation enhanced myocardial afterload. His disease symptoms advanced aggressively, and he passed away even before the heart transplantation. The total illness duration was 19.7 months since parachute implantation.