A remote hypertension management program clinical algorithm

IntroductionHypertension is the leading risk factor for death, affecting over one billion people worldwide, yet control rates are poor and stagnant. We developed a remote hypertension management program that leverages digitally transmitted home blood pressure (BP) measurements, algorithmic care pathways, and patient–navigator communications to aid patients in achieving guideline‐directed BP goals.MethodsPatients with uncontrolled hypertension are identified through provider referrals and electronic health record screening aided by population health managers within the Mass General Brigham (MGB) health system. Non‐licensed patient navigators supervised by pharmacists, nurse practitioners, and physicians engage and educate patients. Patients receive cellular or Bluetooth‐enabled BP devices with which they monitor and transmit scheduled home BP readings. Evidence‐based medication changes are made according to a custom hypertension algorithm approved within a collaborative drug therapy management (CDTM) agreement with MGB and implemented by pharmacists.Using patient‐specific characteristics, we developed different pathways to optimize medication regimens. The renin–angiotensin–aldosterone system‐blocker pathway prescribed ARBs/ACE inhibitors first for patients with diabetes, impaired renal function, and microalbuminuria; the standard pathway started patients on calcium channel blockers. Regimens were escalated frequently, adding thiazide‐type diuretics, and including beta blockers and mineralocorticoid receptor antagonists if needed.DiscussionWe have developed an algorithmic approach for the remote management of hypertension with demonstrated success. A focus on algorithmic decision‐making streamlines tasks and responsibilities, easing the potential for scalability of this model. As the backbone of our remote management program, this clinical algorithm can improve BP control and innovate the management of hypertension in large populations.     

Effects of cilnidipine and L-type calcium channel blockers on renal functions in hypertensive patients: a meta-analysis of the randomized trials

In the present study, we aimed to evaluate the effects of cilnidipine and L-type calcium channel blockers (L-type CCBs) on renal function in hypertensive patients. The randomized controlled trials (RCTs) of cilnidipine and L-type CCBs on hypertension treatment were selected from Pubmed, Embase, Google Scholar, CNKI, Science Direct, Ebsco, Springer, Ovid, Cochrane Library, Medline, VIP and Wanfang databases (from the date of databases’ establishment to September 2014). Data were independently evaluated following the Jadad standard. The percentage changes of serum creatinine (SCr) value, urinary protein excretion (UPE), urinary protein/creatinine ratio (UPCR) and estimated glomerular filtration rate (eGFR) pre- and post-treatment were extracted for the subsequent meta-analysis. The mean difference (MD) and the 95% confidence interval (95% CI) were determined using RevMan 5.3 software.A total of 10 RCTs of high quality were included and analyzed by fixed- or random-effect models. The results indicated that UPE (MD = –36.59, 95% CI: –70.85, –2.33) or UPCR (MD = –46.56, 95% CI: –88.50, –4.62) was significantly reduced by cilnidipine compared with L-type CCBs. However, such significant difference was not detected in reduction of SCr (MD = 0.01, 95% CI: –2.97, 2.98) or eGFR (MD = 1.56, 95% CI: –0.19, 3.31). Compared with L-type CCBs, cilnidipine was more effective in reducing proteinuria or preventing the proteinuria progression. In addition, we did not find significant differences in SCr and eGFR between the two groups.     

Amlodipine and calcineurin inhibitor‐induced nephrotoxicity following allogeneic hematopoietic stem cell transplant

Studies in the renal transplant population have suggested calcium‐channel blockers (CCBs) may protect against calcineurin inhibitor (CNI)‐induced nephrotoxicity. However, this has not been evaluated in the hematopoietic stem cell transplant (HSCT) population. This retrospective study reviews data from 350 consecutive patients who underwent allogeneic HSCT to determine whether amlodipine improved renal outcomes. Subject data included up to one year from CNI initiation. Patients in the amlodipine group (n = 130) received an average of 143 days treatment with amlodipine and experienced a smaller decrease in creatinine clearance (CrCl) through day 180. At day 30, change in CrCl was ?17.4 mL/min in the amlodipine cohort and ?33.8 mL/min in the control (P < 0.001). At day 180, change in CrCl was ?40.9 and ?50.6 mL/min, respectively (P = 0.005). Incidence of hospitalization with acute kidney injury (AKI) was significantly lower in patients receiving amlodipine, 7.7% (10/132) vs 16.4% (36/220) (hazard ratio [HR] 0.44; 95% confidence interval [CI] 0.22‐0.89). Median blood pressure in the amlodipine group remained <132/78 through day 360. Our data support the use of amlodipine for hypertension in the allogeneic HSCT population and provide evidence suggesting that CCBs protect against CNI‐induced nephrotoxicity.     

Angiotensin-Converting Enzyme Inhibitors, Angiotensin II Receptor Antagonists and Calcium Channel Blocking Agents: A Review of Potential Benefits and Possible Adverse Reactions

A review of recent studies suggests that the use of angiotensin-converting enzyme (ACE) inhibitors may be preferred (usually along with a diuretic drug) as initial therapy in several subsets of hypertensive patients (i.e., those with diabetes and nephropathy or with diminished left ventricular function with or without symptoms of heart failure). Limited long-term data are available for the angiotensin II receptor antagonists. The use of nondihydropyridine calcium channel blocking agents (CCBs) appears to reduce reinfarction in patients with ischemic heart disease (however, mortality is not reduced). Long-acting formulas of CCBs appear to decrease congestive heart failure in patients with dilated, but not ischemic, cardiomyopathy and to decrease strokes and arrhythmias in hypertensive subjects. Short-acting agents (primarily those that increase heart rate) may increase coronary heart disease events in hypertensive patients. There is little evidence at present that CCBs offer a major advantage over other antihypertensive agents or that they should be recommended as initial therapy, except in special situations.

(J Am Coll Cardiol 1997;29:1414–21)     

Mechanism of protective effects of Danshen against iron overload-induced injury in mice

Ethnopharmacological relevance

Danshen (Salvia miltiorrhiza) has been widely prescribed in traditional folk medicine for treatment of hepatic and cardiovascular diseases in China and other Asian countries for several hundred years.

Materials and methods

Sixty male mice were randomly divided into five groups: control, iron overload, low-dose Danshen (L-Danshen, 3 g/kg/day), high-dose Danshen (H-Danshen, 6 g/kg/day) and deferoxamine (DFO) groups (n=12 per group). Iron dextran was injected intraperitoneally (i.p.) at 50 mg/kg body weight/day to establish the iron overload model. While control mice received saline, mice of the treated groups simultaneously received (i.p.) injections of L-Danshen, H-Danshen or DFO daily for 2 weeks. At the end of the experiment, changes in alanine aminotransferase (ALT) and aspartate aminotransferase (AST), glutathione peroxidase (GSH-Px), superoxide desmutase (SOD) and malondialdehyde (MDA) were measured, and histological changes were observed by Prussian blue or hematoxylin and eosin staining of the liver. Apoptosis was detected by terminal-deoxynucleotidyl transferase mediated nick end labeling.

Results

Treatment of iron overloaded mice with either low or high doses of Danshen not only significantly attenuated the hepatic dysfunction (ALT/AST levels), decreased the content of MDA and increased the activities of GSH-Px and SOD, it also suppressed apoptosis in hepatocytes. Histopathological examination showed that treatment with Danshen reduced iron deposition and ameliorated pathological changes in the liver of iron overloaded mice.

Conclusions

Danshen demonstrated significant protective effects in the liver of iron overloaded mice, which were at least partly due to the decrease of iron deposition and inhibition of lipid peroxidation and hepatocyte apoptosis.     

Saga of Renin‐Angiotensin System and Calcium Channels in Hypertensive Diabetics: Does it Have a Therapeutic Edge?

Current understanding of the genesis of diabetic vascular disease suggests that vascular complications, such as atherosclerosis and hypertension, are associated with changes in structural and functional parameters. Experimental and epidemiological data suggest that activation of the renin‐angiotensin‐aldosterone system plays an important role in the development of micro‐ and macro‐vascular complications. Most of the negative cardiovascular actions of angiotensin II are mediated through AT₁ receptors, whereas the AT₂ receptors mediate largely beneficial effects. Hence, compared to angiotensin converting enzyme inhibitors (ACEIs), selective AT₁ receptor blockers (ARBs) should provide additional end organ protection via AT₂ receptors activation. Although ACEIs are useful therapeutically, they are being currently displaced by ARBs. Enhanced calcium ion channel activity is reported in vascular smooth muscles from diabetic animal models. Clinical benefits of calcium channel blockers (CCBs) in diabetic hypertensive patients are controversial, but there is increasing experimental evidence for the beneficial effects of dihydropyridine‐type CCBs. Although the treatment of hypertension in diabetics reduces cardiovascular and microvascular complications, the ideal strategy for treating hypertension in diabetics has not been well defined and warrants a combination approach. Only limited clinical data regarding the use of ARBs in combination with CCBs in diabetics are available. The experimental data suggest that combination of a CCB and an AT₁ receptor blocker, or a hypothetical dual blocker of AT₁ receptors as well as of calcium channels would be an ideal regimen. There is, however, no conclusive clinical evidence to support the combined use of these drugs. This review highlights the available experimental data that support the therapeutic benefits of this combination.     

钙通道拮抗剂体外对人精子运动参数的影响

目的　探讨钙通道拮抗剂在体外对人精子运动参数的影响。方法　将不同类型的钙通道拮抗剂在体外与生育男性经上游优化处理的精子分别共同孵育 10、2 0、3 0、60min ,与正常组进行对照研究。采用计算机辅助精子分析系统检测人精子运动参数 (精子活率、精子前向运动百分率、畸形率、平均路径速度、精子侧摆幅度和摆动幅度 )。结果　硝苯地平 (10 μmol/L)在体外对精子活率 (P <0 .0 1)、精子前向运动百分率 (P <0 .0 1)、精子平均路径速度 (P <0 .0 0 1)、精子侧摆幅度 (P <0 .0 1)和摆动幅度 (P <0 .0 1)等指标的差异有非常显著性。结论　人精子细胞中存在L 型电压依赖性钙通道 ,且L 型钙通道拮抗剂可导致男性不育。