Left ventricular hypertrophy and its regression in essential arterial hypertension. A tissue Doppler imaging study

The mitral annulus velocities of Doppler transmitral flow and pulsed-wave tissue Doppler imaging (TDI) were sampled by echocardiography for the assessment of left ventricular (LV) diastolic function in 118 never-treated essential hypertensive patients with normal systolic function and compared with those of 59 normotensive healthy subjects matched for age and sex. A selected group (n = 26) of the hypertensive study population was observed after 1 year of pharmacologic antihypertensive treatment to determine the behavior of TDI parameters in relation to eventual regression of LV hypertrophy (LVH). We found that the TDI early myocardial diastolic wave (E(m)) was significantly lower both in concentric and eccentric LVH. In addition, TDI late myocardial diastolic wave (A(m)) was significantly higher in concentric remodeling and concentric and eccentric hypertrophy. The TDI E(m)/A(m) ratio was significantly lower in all geometric remodeling subgroups. The E/A ratio Doppler transmitral flow velocity measured showed that of the 118 patients, only 32 (25%) could really be discriminated from normal, whereas individual analysis for TDI E(m)/A(m) at the mitral annulus septal level showed that of 118 patients 108 (91%) could be discriminated from normal P < .001). The LV mass was significantly less after 1 year of treatment (LVH regression), and TDI parameters showed a trend toward normalization, in particular of TDI E(m)/A(m) at the annular septal level. Pulsed-wave TDI analysis could enable not only the early assessment of whether a patient is still in an adaptive or compensatory phase before transition to irreversible damage (pathologic phase) but also the detection of precocious LV global diastolic dysfunction. With regard to this, more extensive randomized studies are needed to evaluate the effect of different pharmacologic treatments (calcium antagonists, beta-blockers, angiotensin I and II inhibitors) on TDI parameters.     

The STRAND Chart: A survival time control chart

The STRAND Chart (Survival Time, Risk-Adjusted, N-Division Chart) is a new tool for online risk-adjusted (RA) monitoring of survival outcomes. The chart is drawn in continuous time, making it responsive to change in the process of interest, for example, performance over time of a surgical unit and the procedures that they employ. Though it is difficult to achieve with charts designed for the purpose described, we show that our suggested chart keeps patient ordering intact. We discuss the difficulties maintaining patient ordering poses, making reference to other charts in the literature. Our conclusion is that the best approach to preserving patient ordering on any chart of this nature involves compromising on the fullness of presentation of the recorded data. The chart is divided into N strands, each strand relating to a benchmark patient's survival information at t_n days following treatment, n = 1,2,…,N. We present a simple version of the chart where the strands consist of Bernoulli RA exponentially weighted moving averages, recording RA failure rates at t_n days. It can detect recent process change and historical change. We illustrate the STRAND Chart using a well-known UK post cardiac surgery survival dataset, where the nature of a certain cluster in the data can be seen.     

Effect on Clinical Restenosis of an Ultra‐Thin‐Strut Bare Metal Cobalt‐Chromium Stent Versus a Thin‐Strut Stainless Steel Stent

Objectives

To prospectively compare the impact of ultrathin‐strut cobalt‐chromium (Cro‐Co) bare metal stent (BMS) versus thin‐strut stainless steel (SS) BMS on clinically driven target lesion revascularization (TLR).

Background

Stent characteristics are an important determinant of restenosis. Thinner strut Cro‐Co BMS is associated with a reduction of neointimal formation compared to SS BMS. The advantages of Cro‐Co BMS in a real‐world population is not clear.

Methods

Patients undergoing percutaneous coronary intervention (PCI) with BMS for any reason were enrolled. Patient with multi‐vessel PCI, multi‐lesions PCI, PCI of unprotected left main and coronary grafts were not excluded. They were divided in two groups according to stent type: Cro‐Co or SS group. The primary endpoint was clinically driven TLR at follow‐up.

Results

A total of 383 patients were enrolled: 222 in SS and 161 in Cro‐Co group. During the follow‐up, Cro‐Co patients had a significantly lower occurrence of TLR compared to SS patients (1.9% vs 8.6%, P = 0.006). There were no significant differences for the composite endpoint of death, myocardial infarct, and stroke (4.9% in Cro‐Co group vs 9.5% in SS group, P = 0.119). At multivariate analysis, the variables that were predictors of TLR were: use of SS stent (OR 4.43, P = 0.019) and diabetes (OR 2.84, P = 0.025).

Conclusions

Ultra‐thin strut Cro‐Co BMS is associated with a significant reduction of clinically driven TLR in all comers population with any type of coronary disease complexity. (J Interven Cardiol 2016;29:300–310)

     

Famotidine for healing and maintenance in nonsteroidal anti- inflammatory drug-associated gastroduodenal ulceration

BACKGROUND & AIMS: Nonsteroidal anti-inflammatory drugs (NSAIDs) are strongly associated with gastroduodenal ulceration. How to manage patients with NSAID-associated ulcers is a common clinical dilemma. High-dose famotidine in the healing and maintenance of NSAID-associated gastroduodenal ulceration was therefore evaluated. METHODS: One hundred four patients with rheumatoid or osteoarthritis who had gastroduodenal ulceration received famotidine, 40 mg twice daily. Sixteen patients stopped and 88 continued their NSAID treatment. Ulcer healing was assessed endoscopically at 4 and 12 weeks. Seventy-eight NSAID users with healed ulcers were then randomized to receive 40 mg twice daily famotidine or placebo and underwent endoscopy at 4, 12, and 24 weeks. RESULTS: Cumulative ulcer healing rates at 12 weeks were 89.0% (95% confidence interval [CI], 82.3%-95.7%) for patients who continued NSAID treatment and 100% (95% CI, 82.9%-100.0%) for those who stopped. The subsequent estimated cumulative gastroduodenal ulcer relapse over 6 months for NSAID users who took placebo was 53.5% (95% CI, 36.6%- 70.3%). This was reduced to 26.0% (12.1%-39.9%) in patients taking famotidine (P = 0.011). CONCLUSIONS: High-dose famotidine is effective ulcer healing therapy in patients who stop or continue NSAID treatment and significantly reduced the cumulative incidence of gastroduodenal ulcer recurrence compared with placebo when given as maintenance therapy. (Gastroenterology 1997 Jun;112(6):1817-22)     

BCR-ABL-mediated inhibition of apoptosis with delay of G2/M transition after DNA damage: a mechanism of resistance to multiple anticancer agents

A critical determinant of the efficacy of antineoplastic therapy is the response of malignant cells to DNA damage induced by anticancer agents. The p53 tumor-suppressor gene is a critical component of two distinct cellular responses to DNA damage, the induction of a reversible arrest at the G1/S cell cycle checkpoint, and the activation of apoptosis, a genetic program of autonomous cell death. Expression of the BCR-ABL chimeric gene produced by a balanced translocation in chronic myeloid leukemia, confers resistance to multiple genotoxic anticancer agents. BCR-ABL expression inhibits the apoptotic response to DNA damage without altering either the p53-dependent WAF1/CIP1-mediated G1 arrest or DNA repair. BCR-ABL-mediated inhibition of DNA damage-induced apoptosis is associated with a prolongation of cell cycle arrest at the G2/M restriction point; the delay of G2/M transition may allow time to repair and complete DNA replication and chromosomal segregation, thereby preventing a mitotic catastrophe. The inherent resistance of human cancers to genotoxic agents may result not only by the loss or inactivation of the wild-type p53 gene, but also by genetic alterations such as BCR-ABL that can delay G2/M transition after DNA damage.     

Clonal rearrangement and expression of the T cell receptor beta gene and involvement of the breakpoint cluster region in blast crisis of CGL

A case of lymphoid blast crisis of Ph1-positive CGL is described in which the blast cells had an immature T cell phenotype, clonal rearrangement and expression of the T cell receptor beta gene, and a rearrangement of the breakpoint cluster region (bcr) on chromosome 22. This case therefore provides definite evidence for transformation involving a common myeloid-T lineage progenitor, penetrance of the Ph1 molecular alteration into the T cell lineage, and clonal selection in blast crisis at the level of a committed T lineage precursor.     

Endothelin-1 release from atherosclerotic plaque after percutaneous transluminal coronary angioplasty in stable angina pectoris and single-vessel coronary artery disease

To assess the effects of percutaneous transluminal coronary angioplasty on endothelin-1 (ET-1) release, we assessed ET-1 concentrations at different sites of the coronary circulation in patients submitted to elective procedures. ET-1 levels immediately downstream from the plaque and ET-1 aortocoronary gradient increased significantly after the procedure, which was related to mechanical wall stress in patients only receiving balloons, but not in those undergoing stent percutaneous transluminal coronary angioplasty. No changes were found in the coronary sinus; these results suggest ET-1 release from the plaque rather than an ischemia/reperfusion-related production from the distal myocardium.