Association of worsening arterial stiffness with incident heart failure in asymptomatic patients with cardiovascular risk factors.

We investigated the independent and incremental role of worsening arterial stiffness in new-onset heart failure (HF) in patients with preclinical HF. We retrospectively studied 456 consecutive asymptomatic patients with HF risk factors (hypertension, obesity, type 2 diabetes mellitus, atrial fibrillation and ischemic heart disease) who underwent paired applanation tonometry examinations (median interval of 2.4 years) during 2006-2011. Brachial ankle pulse wave velocity (baPWV) was measured as a surrogate marker of arterial stiffness. Patients were followed up for admission for new-onset HF over a median duration of 4.9 years after the second examination. HF was observed in 30 patients (7%). The change in baPWV (∆baPWV) was significantly associated with hospitalization for new-onset HF, independent of and incremental to comorbidities, renal dysfunction, left ventricular (LV) dysfunction and baPWV at baseline. Even in patients with an LV ejection fraction of ⩾40%, ∆baPWV was significantly associated with hospitalization for new-onset HF after similar adjustments. When the patients were divided into groups based on this cutoff value of ⩾15% ∆baPWV and the generally accepted external cutoff value of ⩾1750 cm s-1 for baseline baPWV, the Kaplan-Meier estimates of the time of hospitalization for new-onset HF showed that a higher rate of HF was associated with higher baPWV at baseline and higher ∆baPWV (P=0.00005). In asymptomatic patients with cardiovascular risk factors, the deterioration in arterial stiffness was associated with hospitalization for new-onset HF, independent of and incremental with the clinical LV function and increased stiffness parameters at baseline.

Heterogeneous Intravascular Ultrasound Findings of Stent Thrombosis.

Objective The underlying mechanisms of stent thrombosis are not completely understood. Methods We experienced 12 definite stent thrombosis cases (1 early, 1 late, and 10 very late) at our hospital from July 2011 to April 2016 and evaluated the possible causes of stent thrombosis by intravascular ultrasound (IVUS). Results Five different potential morphological causes of stent thrombosis (neoatherosclerosis, stent malapposition, stent fracture, edge dissection, and stent underexpansion) were detected by IVUS in 10 cases (83.3%); in 1 of the remaining 2 cases, the discontinuation of antithrombotic drugs resulted in early stent thrombosis without abnormal IVUS findings. Of the 12 stent thrombosis cases, 4 occurred at a bare-metal stent (average time from stent implantation, 106 months); in all 12, significant neointimal hyperplasia was observed on IVUS, and 2 had plaque ruptures at an in-stent or proximal reference. Malapposed stent struts were observed in three very-late stent thromboses, and all of these underwent sirolimus-eluting stent implantation. Stent thrombosis due to mechanical (stent fracture) or procedure-related complications (edge dissection and stent underexpansion) was observed in three cases. Conclusion In patients with stent thrombosis, heterogeneous findings were observed in IVUS. This IVUS case series illustrates the possible mechanisms of stent thrombosis.

Contribution of the long-term care insurance certificate for predicting 1-year all-cause readmission compared with validated risk scores in elderly patients with heart failure.

OBJECTIVES: Readmission is a common and serious problem associated with heart failure (HF). Unfortunately, conventional risk models have limited predictive value for predicting readmission. The recipients of long-term care insurance (LTCI) are frail and have mental and physical impairments. We hypothesised that adjustment of the conventional risk score with an LTCI certificate enables a more accurate appreciation of readmission for HF. METHODS: We investigated 452 patients with HF who were followed up for 1 year to determine all-cause readmission. We obtained their clinical and socioeconomic data, including LTCI. The three clinical risk scores used in our evaluation were Keenan (2008), Krumholz (2000) and Charlson (1994). We used net reclassification improvement (NRI) to assess the incremental benefit. RESULTS: Patients with LTCI were significantly older, and had a higher prevalence of cerebrovascular disease and dementia than those without LTCI. One-year all-cause readmission (n=193, 43%) was significantly associated with all risk scores, receiving LTCI and the category of LTCI. Receiving LTCI was associated with readmission independent of all risk scores (HR, 1.59 to 1.63; all p<0.01). Adding LTCI to all risk scores led to a significantly improved reclassification, which was observed in the subgroup of patients with HF with preserved ejection fraction (≥50%) but not in the subgroup with reduced ejection fraction (<50%). CONCLUSIONS: Possession of an LTCI certificate was independently associated with 1-year all-cause readmission after adjusting for validated clinical risk scores in patients with HF. Adding LTCI status significantly improved the model performance for readmission risk, particularly in patients with HF and preserved ejection fraction.

Usefulness of Intravascular Ultrasound for Predicting Risk of Intraprocedural Stent Thrombosis.

Intraprocedural stent thrombosis (IPST) is a rare complication of percutaneous coronary intervention that leads to poor outcomes; however, the factors contributing to IPST remain largely unknown. Accordingly, we used intravascular ultrasound (IVUS) to examine the lesion characteristics in patients with IPST. We retrospectively analyzed 1,504 consecutive stent-implanted lesions in 1,324 patients (326 with ST-segment elevation myocardial infarction [STEMI], 403 patients with non-ST-segment elevation acute coronary syndrome [NSTE-ACS], and 595 patients with stable angina). Of these, IPST occurred in 5 patients during percutaneous coronary intervention (0.4% per patient; 3 with STEMI, 2 with NSTE-ACS). The IVUS characteristics of plaques that developed IPST were compared with those of controls without the evidence of IPST (non-IPST; n = 15) who were matched by age, gender, lesion location, and clinical presentation (STEMI, NSTE-ACS, or stable angina). All 5 lesions that led to IPST had ruptured plaques with positive remodeling and attenuation. Plaque rupture was also observed in 40% of the non-IPST group. Multiple plaque ruptures in the culprit lesion were more common in the IPST group (80% vs 7%; p <0.01). The maximum cavity area was larger in the IPST group than in the non-IPST group having plaque rupture (4.6 mm(2) [interquartile range, 4.3 to 6.5] vs 2.4 mm(2) [1.8 to 2.9]; p <0.01). In conclusion, we found using IVUS that multiple plaque ruptures with larger cavities more often evolved into IPST.