It is a self-expandable sirolimus-eluting coronary stent system, similar in concept to other self-expanding systems.

Watch the video:

Stentys self-apposition SES


Patients – 152 patients presenting with STEMI.

Design: Patients were randomized to Stentys self-apposing SES (Stentys, Paris, France; n = 90)   vs Resolute zotarolimus-eluting stent (ZES; Medtronic, Santa Rosa, CA; n = 62). Each treatment arm was then randomized to either 4- or 9-month follow-up.

 -Results: On QCA, no differences were observed between the treatment arms just after the procedure for in-stent minimal and mean lumen diameter. In-stent mean lumen diameter was larger at both 4- and 9-month follow-up for Stentys compared with Resolute (3.39 ± 0.46 mm vs 3.13 ± 0.35 mm).

-OCT demonstrated that Stentys SES was associated with fewer malapposed struts (0.07 ± 0.26% vs 1.16 ± 1.59%) and more covered struts (94.32 ± 5.69% vs 89.09± 5.65%) than Resolute ZES at 4 months. Percentage of stents with all struts covered was also higher with Stentys compared to Resolute ZES (33.3% vs 3.8%).

-No differences in malapposition (P = .55) or coverage (P = .81) were seen between the treatment arms in the 9-month cohort.

-Clinical outcomes were low and well balanced between stent groups in terms of MACE (P = .46), TVF (P = .46), and target vessel MI (P = .39).

-Predilatation Needed.

-The device is larger in profile as compared to DES

 Conclusion: Stentys, a self-apposing sirolimus-eluting stent (SES), shows ‘excellent’ apposition over time—better than an existing balloon-expandable drug-eluting stent—in patients with ST-segment elevation myocardial infarction (STEMI). The newer device is associated with faster strut coverage.

Your comments and insight most welcome


Vorapaxar (Zontivity) approved

CardioSource – FDA Approves Vorapaxar to Reduce Heart Attack and Stroke Risks in HighRisk Patients.

The U.S. Food and Drug Administration (FDA) has approved vorapaxar (Zontivity) to reduce the risk for MI, stroke, cardiovascular-related death and coronary revascularization among patients who have previously experienced MI or peripheral artery disease.

Vorapaxar is the first in a new class protease-activated receptor-1 (PAR-1) antagonist drugs

targets thrombin-induced platelet activation.

In patients who have had a heart attack or who have peripheral arterial disease, this drug will lower the risk of heart attack, stroke, and cardiovascular death.

In the study that supported the drug’s approval, Zontivity lowered this risk from 9.5 percent to 7.9 percent over a 3-year period – about 0.5 percent per year.

Adverse effects include excess bleeding and easy bruisability

A 2011 clinical trial (TRA 2P-TIMI 50 Presentation Slides (Morrow))showed vorapraxar, added to other anti-platelet agents (generally aspirin and clopidogrel), reduced the rate of a combined endpoint of heart attack, stroke, cardiovascular death, and coronary revascularization when compared to placebo.

Genetic mutation in Metabolic Syndrome

A Form of the Metabolic Syndrome Associated with Mutations in DYRK1B — NEJM.


A founder mutation was identified in DYRK1B, substituting cysteine for arginine at position 102 in the highly conserved kinase-like domain. The mutation precisely cosegregated with the clinical syndrome. Functional characterization of the disease gene revealed that nonmutant protein encoded by DYRK1B inhibits the SHH (sonic hedgehog) and Wnt signaling pathways and consequently enhances adipogenesis. Furthermore, DYRK1B promoted the expression of the key gluconeogenic enzyme glucose-6-phosphatase. The R102C allele showed gain-of-function activities by potentiating these effects. A second mutation, substituting proline for histidine 90, was found to cosegregate with a similar clinical syndrome in an ethnically distinct family.


These findings indicate a role for DYRK1B in adipogenesis and glucose homeostasis and associate its altered function with an inherited form of the metabolic syndrome.

Renal artery denervation in post-stenting patients


A new study published in Journal of endovascular therapy (2014;21:181–190) has evaluated the efficacy of renal denervation therapy for hypertension refractory to renal artery stenting.

The study included ten patients (6 women; mean age 70.0±5.1 years) with an office systolic blood pressure >160 mmHg despite taking ≥3 antihypertensive drugs and uni- or bilateral renal artery stenting. These patients were treated with RDN. Radiofrequency (RF) energy was delivered to the native segment of the artery keeping a 5-mm safe distance from the stented segments. Standardized office and ambulatory blood pressure measurements, medication, and renal assessment, including renal duplex ultrasound and renal function, were determined at baseline and on follow-up to 12 months.


Office BP  (systolic/diastolic) at baseline was 190.0±20.4 / 84.2±10.1 mmHg. It decreased to 171.1±28.7 / 82.2±8.7, 165.5±28.4 / 76.1±7.4, and 158.3±14.2/ 75.5±9.5 mmHg (p<0.01) at 3, 6, and 12 months after RDN, respectively. Average ambulatory BP (systolic/diastolic) after 6 and 12 months decreased by −7.6/ −3.1 and −11.3 / −5.1 mmHg (p<0.05).

There was no renal artery (re)stenosis, dissection, or aneurysm within 12 months.

Creatinine, cystatin C, and glomerular filtration rate remained unchanged.

Urine albumin excretion decreased in 4/10 patients.

Renal resistive indices improved in native, but not in stented renal arteries within the follow-up period.

RF-based RDN can be safely and effectively delivered in patients with resistant hypertension and previous renal artery stenting.”


According to a study published online ahead of print in the Journal of American college of cardiology ,patients with acute coronary syndromes (ACS) undergoing percutaneous coronary intervention (PCI) face increased risk of early stent thrombosis in the presence of high thrombus burden with certain pathological traits or suboptimal stenting.

Researchers evaluated 67 stented coronary lesions from 59 patients who presented with ACS and died within 30 days of implantation (between 2004 and 2012).

Early stent thrombosis was identified in 37 lesions from 34 patients (58%), all of whom died of stent-related causes. Of 25 patients without stent thrombosis, cause of death was stent-related in 3 (distal dissection, coronary perforation, and side branch occlusion secondary to stenting). ECG readings at the time of diagnosis revealed STEMI in 16 patients and NSTEMI in 13 patients.

All 33 patients for whom pathological information on the myocardium was available had MI on histologic examination. 

Lesion Characteristics Implicated 

No differences emerged between lesions with (n = 37) or without (n = 30) stent thrombosis in terms of stent location in the coronary tree, duration of the implant, stent type (BMS vs DES or among DES types), number of stents or total stented length, or the underlying pathological findings (eg, plaque rupture, erosion, or calcified nodule).

However, in the stented segment, the maximum index thrombus thickness at the site of greatest thrombus burden was larger and necrotic core prolapse and occlusive thrombus in the side branch were more common in thrombotic lesions compared with patent lesions. Stenting in a false lumen secondary to medial dissection was numerically higher in thrombotic lesions (table 1).

Table 1. Lesion Characteristics: Thrombosis vs Patent

(n = 37 lesions)
(n = 30 lesions)
P Value
Maximum Index Thrombus Thickness, mm 0.22 0.07 0.001
Necrotic Core Prolapse 70% 43% 0.045
Side Branch Occlusion 22% 3% 0.035
False Lumen Stenting 8% 0 0.25

In nonstented segments proximal and distal to the stented segments, severe stenosis (> 75% cross-sectional narrowing), necrotic core prolapse, and medial dissection were more common in thrombotic than patent lesions, but the differences did not reach statistical significance.


Comparison of culprit and nonculprit sections within lesions showed that the extent of necrotic core prolapse, medial tear, and incomplete apposition was higher in sections with thrombus.


In particular, independent predictors of stent thrombosis on multivariate analysis were:

  • Maximum depth of strut penetration (OR 2.3; 95% CI 1.3-4.3; P = 0.006)
  • Percentage of struts with medial tear (OR 1.8; 95% CI 1.3-2.4; P = 0.001)
  • Percentage of struts with incomplete apposition (OR 1.8; 95% CI 1.4-2.4; P < 0.001)

In addition, plaque rupture was more common in arterial sections with vs without stent thrombosis (OR 2.2; 95% CI 1.5-3.2; P < 0.001).



Careful Technique, Improved Stent Designs May Help


The findings emphasize the potential role of intracoronary imaging in describing the underlying plaque, quantifying the lesion extent, and assessing procedural results in terms of stent apposition.


Improvements in stent design may help reduce stent thrombosis risk.


Finally, the contribution of thrombus burden to the development of stent thrombosis reinforces the importance of potent antiplatelet and anticoagulant strategies



Study Details


Age, sex, indication for PCI, and past medical history were similar between subjects with and without stent thrombosis.




1. Nakano M, Yahagi K, Otsuka F, et al. Causes of early stent thrombosis in patients with acute coronary syndrome: an ex vivohuman autopsy study. J Am Coll Cardiol. 2014;Epub ahead of print.

2. Windecker S, O’Sullivan CJ. Mitigating the risk of early stent thrombosis [editial]. J Am Coll Cardiol. 2014;Epub ahead of prin

CRT – the expanded indications

FDA Approves Medtronic CRT Devices for Mild HF With AV Block. This approval is based on the  BLOCK-HF trial. The approval expands the labeling on the defibrillating and pacing-only cardiac resynchronization therapy devices (CRT-D and CRT-P, respectively), which until now had been approved only for heart-failure patients with LVEF <35% and prolonged QRS intervals. The BLOCK-HF indications included a different niche of patients, those with first-, second-, or third-degree AV block, NYHA class 1-3 heart failure, and LVEF <50%. Read more @
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The unheard-of symptom – Bendopnea

Characterization of a Novel Symptom of Advanced Heart Failure: Bendopnea

JCHF. 2014;2(1):24-31. doi:10.1016/j.jchf.2013.07.009

Objectives:  This study sought to examine the frequency and hemodynamic correlates of shortness of breath when bending forward, a symptom that has been named by the newly coined term “bendopnea.”

Background:  Many heart failure patients describe bendopnea such as when putting on their shoes. This symptom has not previously been characterized.

Methods: This was a prospective study of 102 subjects with systolic heart failure referred for right-heart catheterization. Time to onset of bendopnea was measured prior to catheterization. Forty-six subjects also underwent hemodynamic assessment when sitting and bending. Hemodynamic profiles were assigned on the basis of whether pulmonary capillary wedge pressure (PCWP) was ≥22 mm Hg and cardiac index (CI) was ≤2.2 l/min/m2.

Results: Bendopnea was present in 29 of 102 (28%) subjects with median (25th, 75th percentiles) time to onset of 8 (7, 11) seconds. Subjects with bendopnea had higher supine right atrial pressure (RAP) (p = 0.001) and PCWP (p = 0.0004) than those without bendopnea but similar CI (p = 0.2). RAP and PCWP increased comparably in subjects with and without bendopnea when bending, but CI did not change. In those with, versus without, bendopnea, there was more than a 3-fold higher frequency of a supine hemodynamic profile consisting of elevated PCWP with low CI (55% vs. 16%, respectively, p < 0.001) but no association with a profile of elevated PCWP with normal CI (p = 0.95).

Conclusions: Bendopnea is mediated via a further increase in filling pressures during bending when filling pressures are already high, particularly if CI is reduced. Awareness of bendopnea should improve noninvasive assessment of hemodynamics in subjects with heart failure.