High blood pressure is a leading modifiable risk factor cardiovascular disease (CVD) mortality which is why controlling this has become such a big focus for so many healthcare providers. The US currently uses a treat-to-target strategy. Europe on the other hand uses a benefit-based, tailored treatment strategy in which therapy is initiated for patients with high estimated CVD risk. Both of these emphasize that the goal of controlling blood pressure is not to lower it but to avoid CVD events. The team in this study used models to simulate adults ages 30 to 70 in divers populations. The study had three groups, the US method, the European method, and a hybrid of the two.
It turns out that the study showed that the treat-to-target would be the best model to use in both China and India to allow for the most decrease in risk for CVD related events. Less people would be treated under the other system although treatment strategies would be similar.
Basu S, Yudkin JS, Sussman JB, Millett C, and Hayward RA. Alternative strategies to achieve cardiovascular mortality goals in china and india. Circulation. 2016;133:840-48.
A rare complication of acute pulmonary embolism is chronic thromboembolic pulmonary hypertension which is characterized by fibrothrombotic obstructions of large pulmonary arteries in conjunction with small-vessel arteriopathy. The usual treatment for this is a surgery, pulmonary endarterectomy, but in patients who cannot be operated on, they can be treated with medicine. This study compares the effects and outcomes between two groups, one including pateints who receive an operation for their chronic thromboembolic pulmonary hypertension while the other group was only treated medicinally. This is the first study to take a prospective, large-scale, international registry of newly diagnosed patients with CTEPH and include patients who are operated on and those who are not. The most significant thing about it is how that it was long-term.
It turned out that sixty percent of patients were operated on and forty percent were not operated on either by their own decision or for medical reasons. In total, 143 patients died, 51 of which were operated on and 92 that were not operated on. The significant find was the fact that patients that were operated on had a significantly better long-term survival than not-operated patients. Patients were eight years younger, had higher six minutes walking distance and higher cardiac index for those who were operated on. Survival for not-operated patients at 3 years was on seventy percent compared to eighty-nine percent for those who were operated on. One of the biggest determinants of survival was actually the presence of comorbidities such as cancer, coronary disease, left heart failure, and chronic obstructive pulmonary disease. It is important to note that medically treated patients were sicker than the other patients. Another significant note is that patients were treated off-label with endothelin receptor antagonist or phosphodiesterase-5 inhibitor. The long-term effects of the recently improved drug needs to be further evaluated to see if this could lead to more problems down the road.
While reading this it made me realize that it is very difficult to tell what a medication will do to people over a very long period of time, and it is hard to find this out before many people are already taking it. I wonder what other medications could potentially lead to major problems for patients down the road that we do not know about yet.
Delcroix M, Lang I, Pepke-Zaba J, et al. Long-term outcome of patients with chronic thromboembolic pulmonary hypertension. Circulation. 2016;133:859-71.
Prednisolone (PSL) therapy is currently the gold standard of care treatment for patients with cardiac sarcoidosis (CS), a rare disease in which clusters of white blood cells form in the heart tissue. However, the debate is whether physicians are to continue or discontinue prednisolone therapy in long-term treatment.
In this retrospective study, 111 patients were group, however only 61 were included in the analysis. All of the 61 patients had newly suspected CS based on clinical indications, were without coronary artery disease, and were admitted to a particular institution between 1979-2009.
Of the 61 that were included in the study, 49 patients had continuation of PSL and 12 had PSL discontinuation. After discontinuation of PSL, 5 patients suffered from cardiac mortality. Discontinuation of PSL was associated with significantly higher cardiac fatality than compared to the continuation group (p=0.035). Discontinuation of PSL also contributed to greater percent decrease in left ventricular ejection fraction (LVEF) compared with continued therapy (p=0.037).
From this seemingly small study, the investigators were able to shed some insight into the importance of long-term prednisolone treatment maintenance even with observed cardiac improvement.
Am J Cardiol. 2016;117:966-71.
The role of a pharmacist on an inter-professional health care team and their importance to preventing medication related issues in patients that results in hospital re-admissions has been widely studied and accepted as necessary among pharmacists and providers alike. Despite this, many hospitals and clinics are unable to free up the personnel to include enough clinical pharmacists on teams due to the large time commitment associated with such a position. A new study posted in the North Carolina Journal of Medicine attempted to test the feasibility of a Trainee-Integrated Pharmacy Practice (TIPP) model that would utilize pharmacy residents in a cardiology clinic to perform comprehensive medication services under the supervision of a clinical pharmacist preceptor.
In the pilot study, a clinical pharmacist divided time between three teams comprised of pharmacy residents and technicians in critical, intermediate, and acute care cardiology units. Each team was responsible for rounding with the existing care team at in the units, and would make care plan recommendations, verify medication orders, counseling on high-risk medications, and medication reconciliation with the guidance of their clinical pharmacist preceptor. The study tracked the medication recommendations made by each team, as well as the time commitments made by each member of the team to compare the demands that would be place on individual clinical pharmacists.
The results of the study show that after 30 days, the residents and their preceptor managed to find 512 medication reconciliation issues including necessary drugs omitted, incorrect doses, wrong frequencies, duplicate medications, and discontinued medications still being taken. They also increased the rates of patients receiving anti coagulation counseling by 70%, and recommended 762 clinical changes,an average of about 3.5 per patient, of which 720 were accepted by the care team. These recommended alterations generally involved medication optimization, over a fourth of which were recognized by literature to improve general health outcomes and adverse cardiovascular events. Also, the study found that the teams were active in the clinical care process for an average of 10-12 hours per day, with the assistance of medication history compiled by technicians and a staffed medical record specialist to cut down on time spent for patient profiles. This suggests that the time investment necessary would far exceed one clinical pharmacists ability to provide the same services and speaks to the viability of the integrated trainee team.
This study may open doors on inter professional teams for pharmacy residents in patient care roles that currently are not the standard of practice. The study indicates that utilization of trainee-preceptor teams could alleviate the deficit for pharmacy expertise in the clinical setting that most hospitals do not have the resources for. Do these teams provide the depth of knowledge required for positive clinical changes, or should hospitals only be entrusting these issues to established clinical pharmacists? How do you feel about this?
,, From Pilot to Practice: A Trainee-Integrated Pharmacy Practice Model in Cardiology. N C Med J. 2016; 77: 45-51. doi:10.18043/ncm.77.1.45
I found out about this article through a P4 student who was preparing for a case presentation on rotations. I was pleased to realize that the topic relates to our current anatomy and physiology material and even more so that Dr. Coons authored it!
This article evaluates the use of disopyramide in patients with hypertrophic cardiomyopathy (HCM). Before jumping into how disopyramide works and whether it’s effective (topic of the article), I’ll give some basic background information on the disease state. Hypertrophic cardiomyopathy sounds like a mouthful, but it’s essentially an inherited disease of the heart muscle (myopathy) in which the muscle is enlarged/ thickened (hypertrophic) for no apparent reason. If you remember from the anatomy and physiology lectures, thickened heart muscle can lead to a lot of problems. It makes it more difficult for the heart to work efficiently as the thickening decreases elasticity. About 1 in 500 people have this condition, and about two thirds of those with HCM have obstruction of the left ventricular outflow tract (LVOT). This obstruction occurs when the ventricle contracts and drag force pushes the mitral valve leaflet toward the septum. HCM is typically treated with ß blockers or verapamil, and for those with particularly bad cases that don’t respond to medication therapy, surgery is an option. There is another therapy, however, that has been proven to be effective and safe in those with HCM and LVOT obstruction– disopyramide.
Disopyramide is a class 1A antiarrhythmic, but it can be used off-label as treatment in patients with HCM with LVOT obstruction who do not respond to ß blockers or verapamil. This drug works by slowing phase 0 of the cardiac muscle action potential (remember phase 0 is the opening of sodium channels and rapid influx of sodium). Thus it has strong negative inotropic activity (weakens the force of heart contraction) which slows the outflow from the left ventricle which delays or eliminates the mitral-septal contact responsible for obstruction. A review of 3 clinical studies shows that disopyramide improves heart failure symptoms and reduces the need for surgery in those with HCM and LVOT obstruction who don’t respond to ß blockers or verapamil. There are some concerns with this therapy, however. Its pharmacokinetics are interesting– it has nonlinear, saturable protein binding meaning that it’s hard to predict concentrations of free disopyramide given small increases in plasma concentrations. With this in mind, dosing and monitoring in a hospital setting is important when administering disopyramide. Anticholinergic effects and pro-arrhythmias can occur if therapy is not carefully managed.
While we haven’t covered this disease state nor antiarrhythmics in detail in class, I was glad that I could use my current knowledge to better understand disopyramide and HCM. It’s interesting to see how the conceptual groundwork laid in anatomy and physiology and principles of drug action paves the way toward understanding more complex issues. One thing unclear to me, however, is how a drug like disopyramide can have anticholinergic adverse effects. How does the slowing phase 0 of cardiac action potentials relate to the parasympathetic system?
Verlinden N. J., Coons J. C., Pharmacotherapy. Disopyramide for hypertrophic cardiomyopathy: a pragmatic reappraisal of an old drug. 2015; 35:1164-72