Massive Left Ventricular Hypertrophy With Acromegaly: Hypertrophic Obstructive Cardiomyopathy Phenocopy or Phenotype?

Acromegaly-a rare endocrine disorder-results when a growth hormone-secreting somatotroph pituitary adenoma leads to increased insulin-like growth factor 1 production. Acromegaly is known to cause left ventricular hypertrophy. We present a case of acromegaly with massive left ventricular hypertrophy that was determined to be coexistent with gene-positive hypertrophic obstructive cardiomyopathy. (Level of Difficulty: Intermediate.).

Chewed Versus Swallowed Ticagrelor in P2Y12 Inhibitor-Naïve Patients Undergoing Percutaneous Coronary Intervention.

Purpose: Dual antiplatelet therapy is standard for patients undergoing percutaneous coronary intervention (PCI) with stents. Traditionally, patients swallow the loading dose of a P2Y12 inhibitor before or during PCI. Time to achieve adequate platelet inhibition after swallowing the loading dose varies significantly. Chewed tablets may allow more rapid inhibition of platelet aggregation. However, data for this strategy in patients with stable ischemic heart disease or non-ST-elevation acute coronary syndrome (NSTE-ACS) are less robust. Methods: In this single-center prospective trial, 112 P2Y12-naïve patients with stable ischemic heart disease or NSTE-ACS on aspirin therapy and who received ticagrelor after coronary angiography but before PCI were randomized to chewing (n=55) or swallowing (n=57) the ticagrelor loading dose (180 mg). Baseline variables were compared using 2-sample t-test and chi-squared/Fisher's exact tests as appropriate, with alpha set at 0.05. P2Y12 reaction units (PRU) were compared at baseline, 1 hour, and 4 hours using Wilcoxon rank-sum test. Patients then received standard ticagrelor dosing. Results: After exclusions, P2Y12 PRU in the chewed and swallowed groups at baseline, 1 hour, and 4 hours after ticagrelor loading dose were 243 vs 256 (P=0.75), 143 vs 210 (P=0.09), and 28 vs 25 (P=0.89), respectively. No differences were found in major adverse cardiac events (MACE) or major bleeding at 30 days and 1 year. Conclusions: In patients with stable ischemic heart disease or NSTE-ACS, chewing rather than swallowing ticagrelor may lead to slightly faster inhibition of platelet aggregation at 1 hour with no increase in MACE or major bleeding.

Microstructure and physical changes in the Mexican cooked lamb meat barbacoa made with chilled and frozen meat.

Longissimus dorci (LD) samples of different origin (imported and domestic) with pre-treatments (imported meat stored at -18°C for 6months, domestic meat stored at -18°C for 10days, and domestic meat stored at 4°C for 24h) were cooked as barbacoa and frozen using two treatments (air blast and liquid immersion) and then evaluated after 30days of storage. The results showed that the origin and pre-treatment of meat affected L*, a*, instrumental texture and microstructure; that the storage time affected pH, aw, b* and microstructure; and that the freezing treatments did not affect the meat. Overall, the frozen cooked lamb dish barbacoa could present some problems at the conservation stage due to an increase in pH, aw and changes in microstructure; however, the physical traits (color and texture) remained mostly unchanged and depended more on the quality of the raw meat.

Endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation.

Vascular endothelial dysfunction occurs during the human aging process, and it is considered as a crucial event in the development of many vasculopathies. We investigated the underlying mechanisms of this process, particularly those related with oxidative stress and inflammation, in the vasculature of subjects aged 18-91 years without cardiovascular disease or risk factors. In isolated mesenteric microvessels from these subjects, an age-dependent impairment of the endothelium-dependent relaxations to bradykinin was observed. Similar results were observed by plethysmography in the forearm blood flow in response to acetylcholine. In microvessels from subjects aged less than 60 years, most of the bradykinin-induced relaxation was due to nitric oxide release while the rest was sensitive to cyclooxygenase (COX) blockade. In microvessels from subjects older than 60 years, this COX-derived vasodilatation was lost but a COX-derived vasoconstriction occurred. Evidence for age-related vascular oxidant and inflammatory environment was observed, which could be related to the development of endothelial dysfunction. Indeed, aged microvessels showed superoxide anions (O(2)(-)) and peroxynitrite (ONOO(-)) formation, enhancement of NADPH oxidase and inducible NO synthase expression. Pharmacological interference of COX, thromboxane A(2)/prostaglandin H(2) receptor, O(2)(-), ONOO(-), inducible NO synthase, and NADPH oxidase improved the age-related endothelial dysfunction. In situ vascular nuclear factor-kappaB activation was enhanced with age, which correlated with endothelial dysfunction. We conclude that the age-dependent endothelial dysfunction in human vessels is due to the combined effect of oxidative stress and vascular wall inflammation.

Stent fracture, an incidental finding or a significant marker of clinical in-stent restenosis?

BACKGROUND: The predictors and clinical significance for stent fracture (SF) in drug-eluting stents (DES) remain unknown. We identified procedural factors leading to SF and its clinical consequences in DES. METHODS: Percutaneous coronary interventions were performed on 3,920 patients with DES over 12 months. In-stent restenosis (ISR) of DES was observed in 188 cases with 121 cases (64.4%) receiving a sirolimus-eluting stent (SES) and 67 (35.6%) a paclitaxol-eluting stent (PES). RESULTS: SF was identified in 35 (18.6%) of the 188 cases. The 35 cases were then compared with 153 cases of ISR without angiographic evidence of SF. SF was identified in 29 (23.9%) SES compared with 6 (9.0%) in PES (P < 0.05). With univariate analysis, additional factors associated with SF included longer mean stented segment length, male gender, overlapping stents, vessel segment angulation >75 degrees , and more stents (all P < 0.05). With multivariate adjustment, three factors, i.e., stenting on a bend >75 degrees (OR = 13.8, 95%CI 3.7 to 51; P < 0.001), SES (OR = 4.1, 95%CI 1.3 to 13.4; P < 0.018) and overlapping stented segments (OR = 3.9, 95%CI 1.1 to 14.1; P < 0.041) were statistically significant independent predictors of SF while larger stent diameter was protective (OR = 0.14, 95%CI 0.04 to 0.70; P < 0.017). CONCLUSION: SF proved to be associated with angiographically-documented clinical ISR. Although the exact mechanism is unknown, factors that appear to play a negative role in SF include vessel tortuosity, use of SES and overlapping stents. Larger stent diameter was protective. Further studies are needed to better define the factors important in the mechanism of SF.

Biventricular pacing and QT interval prolongation.

INTRODUCTION: The purpose of this study was to examine BiV pacing-dependent changes in QT interval and the related potential for proarrhythmia. Biventricular (BiV) pacing has emerged as a promising therapy for patients with advanced congestive heart failure (CHF) and bundle branch block (BBB). METHODS AND RESULTS: One hundred and seventy-six consecutive patients (123 men and 53 women; mean age 67 +/- 16 years) with ischemic (n = 128) or nonischemic (n = 48) cardiomyopathy in New York Heart Association Class II (8%) or III (92%) CHF (ejection fraction 24 +/- 9%) underwent atrial synchronous BiV pacing. The QRS, QT, and JT intervals were measured at 30 minutes after initiation of BiV pacing, at 24 hours, and at 1 month postimplant. QT interval was defined as the time interval between the initial deflection of the QRS complex and the point at which the T wave crossed the isoelectric line. At baseline, the average QRS duration was 178 +/- 10 ms, attributable to left BBB (n = 158) or intraventricular conduction delay (n = 18). BiV pacing resulted in a small but statistically significant reduction in QRS duration (148 +/- 9 ms during BiV pacing vs 178 +/- 10 ms at baseline [P < 0.0001]), yet the QT increased to 470 +/- 34 ms with BiV pacing versus 445 +/- 32 ms at baseline [P < 0.0001]). The JTc interval during BiV pacing was significantly shorter than during LV pacing (290 +/- 9 ms vs 320 +/- 20 ms, P < 0.0001). During a mean follow-up of 24 +/- 6 months, one patient developed recurrent torsade de pointes. That was eliminated once left ventricular pacing was discontinued. CONCLUSION: Biventricular pacing prolongs QT interval. However, the occurrence of torsade de pointes is uncommon.

Hepatic artery stenosis after liver transplant, managed with percutaneous angioplasty and stent placement.

Hepatic artery stenosis is a recognized vascular complication of orthotopic liver transplant that carries significant morbidity and mortality. The authors present a case of hepatic artery stenosis in a 50-year-old female successfully treated with balloon angioplasty and stent. This case report highlights the importance of percutaneous intervention as a preferred treatment option in patients with hepatic artery stenosis post-orthotopic liver transplant.

Elective percutaneous coronary intervention without on-site surgical backup: a community hospital experience.

CONTEXT: The American College of Cardiology guidelines consider elective percutaneous coronary intervention (PCI) without on-site surgical backup (OSB) a Class-III indication. OBJECTIVE: Our objective was to determine the safety of elective PCI without OSB. DESIGN: The study is a prospective analysis of a cohort of patients who underwent elective PCI without OSB at our institution. All patients were at our community satellite institution in Beloit, Wis. Three hundred twenty-one elective interventions were performed (mean age 64 +/-12, 68% male). The prevalence of diabetes and hypertension was 28% and 82.5% respectively. INTERVENTION: A predefined protocol was designed to transfer patients to a cardiac surgical facility if necessary. An experienced interventional cardiologist reviewed the diagnostic angiograms. Patients with complex lesions were excluded from the study. MAIN OUTCOME MEASURE: Any procedure-related death or emergency coronary artery bypass graft surgery. RESULTS: Three hundred eighty-two vessels were stented. Multi-vessel intervention was performed in 61 patients (19%). Only 5% of lesions were type C. Four hundred thirty-seven stents were deployed. IIb-IIIa inhibitors were used in 77 (24%) cases. Procedural success was 99.7%. There were no deaths, myocardial infarctions nor need for urgent target vessel revascularization at 6 months. CONCLUSION: With careful patient/lesion selection, an experienced interventional cardiologist and a predefined transfer protocol, elective PCI without OSB can be performed safely.

Endovascular treatment of peripheral vascular disease.

An estimated 10 million people in the U.S. have symptomatic peripheral arterial disease (PAD); 20 to 30 million have asymptomatic PAD. The prevalence of intermittent claudication increases with age, affecting >5% of patients over 70. The incidence of claudication doubles or triples in patients with diabetes. As people grow older, symptoms from peripheral vascular disease increasingly limit daily activity. Until recently, vascular surgical procedures were the only alternative to medical therapy in such patients. Today, advances in minimally invasive percutaneous interventions have made endovascular procedures the primary modality for revascularization in most patients. Compared with open surgical procedures, endovascular interventions offer comparable or superior long-term rates of success with very low rates for morbidity and mortality. Furthermore, most of these interventions are performed on an outpatient basis, reducing hospital stays considerably. In this monograph we discuss current endovascular interventions for treating occlusive PAD, aneurysmal arterial disease, and increasingly common venous occlusive diseases.

A case of popliteal stent fracture with pseudoaneurysm formation.

We describe a case of angiographically documented stent fracture and pseudoaneurysm formation in a patient with femoropopliteal disease, which was successfully treated with deployment of an endovascular stent graft. Technical aspects of the procedure are discussed and the experience with stent fractures previously reported in the literature is reviewed.

Predictors and prognostic value of myocardial injury following stent implantation.

BACKGROUND: Troponin I concentrations are frequently elevated following percutaneous coronary intervention (PCI) even in procedures without complications and are considered, by some, as predictive of long-term morbidity and mortality. We assessed whether post-PCI troponin I concentrations bore any relationship to clinical, angiographic and in-laboratory minor adverse events indicative of myocardial injury and evaluated, in follow-up, whether these levels are useful as a predictive markers of adverse events. METHODS: Patients (n=147) who were scheduled for PCI for stent placement were prospectively studied. In-laboratory events recorded were protracted chest pain, electrocardiographic changes, slow flows, dissections and lateral branch affectation. Troponin I and creatinine kinase MB fraction (CK-MB) mass were measured at baseline and post-procedure. Mean clinical follow-up was for 10.4+/-3.6 months. RESULTS: During PCI, at least one adverse event occurred in 34% of patients and, in 38% of them, there was an elevation of troponin I as compared to 5.1% of those patients without any adverse event (relative risk=7.4; P<0.001). Elevation of troponin I concentrations occurred in 16.3% of all patients, 79.2% associated with an AE. CK-MB was elevated in 15.6% of patients. On multivariate analysis, protracted chest pain, lateral branch involvement and slow flow remained statistically significant in relation to post-procedure elevations of troponin I concentrations. Clinical follow-up showed a poorer prognosis in patients who had had elevated troponin I concentrations. CONCLUSIONS: In-laboratory adverse event predict elevated post-procedure troponin I concentrations which are associated with myocardial injury. These elevations, in turn, predict poorer medium-term clinical outcomes.

Effect of glycaemic control on the vascular nitric oxide system in patients with type 1 diabetes.

OBJECTIVE: The mechanisms underlying the relationship between the vascular complications of diabetes and the glycaemic control are not well understood. We tested whether glycaemic control influences the functioning of the nitric oxide system in type 1 diabetic patients and the role for oxidative stress. METHODS: The changes in the forearm blood flow after the infusion in the brachial artery of NG-monomethyl-l-arginine, methacholine, methacholine plus superoxide dismutase, and nitroprusside were evaluated using strain gauge plethysmography in 14 healthy subjects and 24 patients with type 1 diabetes (12 with HbA(1c) < 7.5%; 12 with HbA(1c) > or = 7.5%). After adjusting insulin treatment, the vascular studies were repeated in the initially poorly controlled patients (HbA(1c) > or = 7.5%). RESULTS: Compared with healthy people, impaired vascular responses to NG-monomethyl-l-arginine (P = 0.0001), methacholine (P = 0.007) and nitroprusside (P = 0.0015) were found in the patients with type 1 diabetes and a poor glycaemic control (HbA(1c) >/= 7.5%), but not in subjects with good control (HbA(1c) < 7.5%). Superoxide dismutase improved the responses to methacholine only in those patients with poor control (P = 0.0037). After the adjustment of the insulin treatment in poorly-controlled patients, the responses improved and the effect of superoxide dismutase disappeared only in the patients that achieved good control (n = 9), but not in those who remained poorly-controlled (n = 3). CONCLUSIONS: In patients with diabetes type 1, glycaemic control determines the functioning of the NO system by a reversible mechanism involving superoxide anions. This finding provides an explanation of the relationship between glycaemic control and vascular complications in diabetes.