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Erectile dysfunction treatment course usually depends on the severity of the case and the underlying conditions and causes. According to recent statistics, about 50% of men aged between 40 and 70 suffer from some degree of ED. This information may sound terrible to younger men, but good news is that only each 10th is fully unable to reach and maintain erections. ED therapy usually implies taking drugs, although there are a few other methods: from lifestyle changes to surgeries. In this article we are going to consider ED therapy with medications.

Does ED therapy depend of its causes?

It is strongly recommended to consult your physician and pass a few laboratory tests to help identify the reason of ED. There are 5 major health problems that frequently are to blame for erectile dysfunction symptoms. In this article by My Canadian Pharmacy you can learn more about them. In some cases, the erection problems can be caused not by a disease itself, but by medications for its treatment. Important: never interrupt a prescribed treatment course without informing your doctor, even if you found symptoms of ED caused by this drug. A qualified healthcare specialist can offer alternatives or change your treatment plan.

To resume: before choosing tablets for ED treatment (or along with choosing them), healthcare providers recommend health screening for ED causes. In case you take antidepressants or other drugs that may cause troubles with having erection, visit your doctor for a competent advice on drug interaction and necessary therapy adjustments.

Which drug to choose for erectile dysfunction?

The group of medications used for ED treatment is called Phosphodiesterase-5 (PDE-5) inhibitors. They are used worldwide, are very effective and have few side effects. PDE-5 inhibitors work by increasing the blood flow to genitals during arousement. This type of drugs does not work without sexual stimulation.

The most important generic names for PDE5 inhibitors for erectile dysfunction treatment are:

• sildenafil – usually known under the brand name Viagra
• tadalafil – known under the brand name Cialis
• vardenafil – known under the brand name Levitra
• avanafil – known under the brand name Spedra

What is the difference between the abovementioned 4 drugs for erectile dysfunction treatment? Healthcare specialists say that for new patients it requires trying different ones to evaluate their effect.

The first option usually prescribed by the doctor is Sildenafil (Viagra). This medication has longest been on the market; a lot of research is carried out to study the side effects and interactions of Sildenafil. Patients suffering from side effects of Viagra, are usually prescribed Avanafil (Stendra).

Sildenafil, Vardenafil and Avanafil show effectiveness the next 8 hours after administration, while the action of Tadalafil is much longer – patients report about 36 hours. This feature of Tadalafil is the reason why it is also known under the name “weekend pill”.

Depending on the active ingredient of the pill and the dose, it should be administered about 30-60 minutes before the planned intercourse.

Taking an ED medication after a substantial meal may increase the time of absorption, so it may take longer to notice the effect. The most important rule of ED treatment with PDE5 inhibitors is 1 pill per 24 hours.

Which ED medication is best?

Each of abovementioned drugs has its own benefits and disadvantages and its own mechanism of action. The choice should be entrusted to the healthcare provider. The doctor takes this decision, considering you overall sexual activity and previous experience with ED treatment drugs.

Viagra, Levitra, Cialis and Stendra are effective in more than 70% of cases. Lack of effect may happen due to individual insensitivity or due to one of the following reasons:

• the medication hasn’t started working, i.e. you just haven’t waited long enough;
• the medication has already stopped working (the dosage was taken more than 8 hours ago for Viagra and Levitra and more than 36 hours ago for Cialis);
• your case requires a higher dosage;
• it is necessary to have more sexual stimulation for you to get an erection even with the help of medications.

Nevertheless, the main challenge to obtaining the best ED drug may depend on health insurance or costs. Shopping at local pharmacies may be very expensive, the price for ED medications can be as high as $15-20 per pill.

To be able to hit limits and afford really working medications, you may look for a trusted online pharmacy to shop generic medications for erectile dysfunction treatment.

Side effects and precautions

• PDE5 inhibitors have relatively few side effect, but they do have some, and patients diagnosed with ED should be aware of them.
• Tell your doctor, if you have any cardiovascular disease, even suspected. Discuss risks and benefits of regular sexual activity with you GP.
• Peyronie’s disease, any risk or priapism (painful long-lasting erection), taking alpha-blockers – are also a reason to consult your doctor before taking ED medications.

Important: PDE5 inhibitors should not be combined with drugs containing nitrates (also known as “poppers”, often used for heart diseases treatment.) This combination may put your health at risk.

Contraindications to PDE5 inhibitors intake:

1. Low blood pressure;
2. Strokes in the past;
3. Non-arteritic anterior ischaemic optic neuropathy;
4. In case you suffer from unstable angina or are prone to heart attack;

The most common side effects from taking Viagra, Cialis, Levitra or their generics are:

• Headaches (from mild to severe);
• Increased blood flow to the face (flushing);
• Stuffy nose;
• Nausea and vomiting;
• Vision disturbances;
• Muscle and joint pain.

However, the side effects are slightly different for each drug. Muscle and joint pain side effect is more common for Cialis than for other medications from the list. Levitra and Viagra are more likely to provoke temporary blue-tinged or disturbed vision.

Common mistake in taking ED medications

There are many patients who report about poor effect of ED drugs or claim they don’t work at all. In some cases, this may happen due to improper use of the medication. The most widespread misconception is that ED drugs work as an on/off button for erections. Of course, they don’t and don’t have to. Sexual stimulation and some foreplay are required. And this makes ED medications safe as the erection is achieved when necessary and customers are not likely to get in awkward situations.

How to cut the costs of ED treatment?

The costs per pill may significantly vary from state to state. They also depend on the dosage, packaging and other aspects. It is well-known that the price for branded Viagra, Levitra and Cialis is much higher than for generics, which can be of excellent quality when purchased at a trusted online-pharmacy.

Here are a few more tips:

• Shop for future use: larger packages allow saving up to 40%!
• Ask your doctor, if it is possible to split pills: you may save on buying higher dose and split the pills.
• Learn more about special offers and promotion of the pharmacy you shop at.
• Compare the prices at online pharmacies and pay attention to delivery terms: some online pharmacies offer free shipping for orders from 50-100 dollars.

How to improve the effect from ED medications?

Here are a few tips of how to help ED pills work better and to improve your health and decrease ED symptoms:

1. Lose weight in case you are overweight. Healthy diet and limiting of fatty foods helps to improve the cardiovascular health and protect blood vessels from clogging – all that leads to better and stronger erections.
2. Give up smoking. Smoking is associated with impaired blood flow due to increased blood viscosity, poor vessel elasticity and, as a result, weak erections.
3. Cut back your alcohol consumption. Most of the ED treatment pills don’t make a good combination with alcohol. Research say that excessive consumption of alcohol leads to decreased sexual activity.
4. Add some physical exercise. Regular movement, walking a few hours per day and exercising improves the blood flow, especially in the pelvis, where the blood can’t move freely as we sit most of the time throughout the day. Besides, exercising decreases risks of heart diseases.
5. Avoid stress. This may sound unreal, but try to replenish your emotional and mental reserves after a stressful day and do not use stimulators, such as drugs, alcohol, smoking or caffeine. Give yourself a peaceful rest, enjoy the silence occasionally. Stress hormones block the mechanisms responsible for sexual activity as the nature decided that stressful time is not suitable for reproduction.

Although, there are no breathtaking research results, proving that healthy lifestyle can beat ED, but it can’t hurt anyway.

Sooner or later each of us comes to the necessity of buying medicines. According to the statistics, the age of those who begin taking medicines regularly is much lower than ever before. This is the sad statistics. Illnesses do not make good to our organisms and they do not prolong our ability to live. They cut it down greatly. So, it is advisable to keep to healthy habits and do much sport.

The advice is wonderful but it turns out to be absolutely impossible with today’s daily routines. People have to work much and, thus, they lack time to cook healthy food and stay in their stuffy offices for hours. Moreover, they sometimes even lack time to go out to the local pharmacy and buy pills for health improvement.

I am one of those extremely busy personalities that literally live in the Internet. I work here, socialize, find friends, take part in different sorts of things and even do shopping. I do not have enough time for walking to the markets and cafes, let alone sport gyms. That is why it is so important for me to be able to do shopping at a pharmacy through the Internet as well. Recently I noticed certain disorders in functioning of some of my most important organ. You know what… Well, I do understand that drugs are usually bought at pharmacies.

But how can I stand in a line with people that buy medicines for their headaches, coughs and painkillers, and I suddenly pronounce ‘Viagra, please…’ or ‘Something to treat hemorrhoids, please…’ I already hear them giggling behind my back and a young drugstore assistant-girl trying to behave naturally. That is awfully embarrassing! That is why I sat about finding an online pharmacy which could deliver the drugs I need right to my house (because at the post office they can read the name of the parcel and it is not going to be pleasant as well). I thought I could bear the expression of the courier’s face at my doorstep. How happy I was when I noticed neither of any possible reaction on his face when he actually delivered my parcel. Thanks Goodness, I found the way out with online Canadian pharmacy.

I Became Regular of the Online Canadian Health&Care Mall

They offer so many advantages in comparison with shopping at land based drugstores that it becomes just nonsense to go on attending the latter ones. You switch on your PC or laptop or tablet whenever you can do it (independently of working hours because online stores do not have those) and look for the medicines you need. My only advice would be to read the instructions to make sure that the chosen medicine is really the one you need and then you are free to make an order with a single click.

When It Comes to Pricing Policy…

The prices are low. To be more precise, they are even lower than you think. You can check out that fact without going too far. Just visit several other online drugstores, open webpages containing information on the certain drug and look through the prices of the same medicines. A pleasant surprise, isn’t it? This online pharmacy has a transparent policy so that the clients could know what they pay for and how much.

Privacy Guaranteed? I Swear It Is!

This feature is extremely important when you are trying to purchase one of those medicines mentioned above. Viagra-like drugs will be delivered right to your house. The couriers are very polite and the delivery is really fast. So, you’ve got my recommendations and now can feel absolutely comfortable to order from Canadian Health and Care Mall – http://www.canadianhealthcaremalll.com.

In recent decades, clinical and public health efforts to reduce the burden of cardiovascular disease have emphasized the importance of calculating global, short-term (generally 10-year) risk estimates. However, the majority of adults in the United States who are considered to be at low risk for cardiovascular disease in the short term are actually at high risk across their remaining lifespan. Estimates of the lifetime risk of cardiovascular disease provide a more comprehensive assessment of the overall burden of the disease in the general population, now and in the future, because they take into account both the risk of cardiovascular disease and competing risks (e.g., death from cancer) until participants reach an advanced age. Such estimates can help guide public health policy, allowing projections of the overall burden of cardiovascular disease in the population.

Most estimates of the lifetime risk of cardiovascular disease have been derived from analyses restricted to risk factors measured at a single age in a predominantly white population.6,7 These estimates do not account for the potential effects of birth cohort that may arise from secular changes in risk-factor levels8,9 or for the widespread use of medical treatment, which has translated into marked reductions in rates of cardiovascular events in the United States.10

The Cardiovascular Lifetime Risk Pooling Project was designed to collect and pool data from numerous longitudinal epidemiologic cohort studies conducted in the United States over the past 50 years. This pooling approach provides an opportunity to calculate estimates of the lifetime risk of cardiovascular events according to age, sex, race, and other risk factors across multiple birth cohorts that would not be feasible within any one data set alone.

Study Sample

We included data sets in the Cardiovascular Lifetime Risk Pooling Project if they met the following criteria: they represented either community-based or population-based samples or large volunteer cohorts, they included at least one baseline examination with direct measurement of physiological and anthropometric (e.g., weight) variables, and they included 10 or more years of follow-up for fatal or nonfatal cardiovascular events or both. Data from 18 unique cohorts were included in the study, 17 of which were included in the pooled analysis. Because of the large size of one study, the Multiple Risk Factor Intervention Trial (MRFIT), relative to the other 17 studies, this cohort was analyzed separately. All data were appropriately de-identified, and all study protocols and procedures were approved by the institutional review board at Northwestern University.

Ascertainment of Baseline Measures and Follow-up Events

The protocols used to obtain data on demographic characteristics, personal and medical history, physical examination, laboratory results, and follow-up procedures for ascertainment of vital status and events for all cohorts included in the study have been published elsewhere. Blood pressure and serum cholesterol levels were measured directly in all participants; data on smoking status were self-reported, as were data on diabetes status, the latter derived from records of self-report, use of medication for diabetes, or both. Events were ascertained with the use of strategies selected by each cohort’s investigator group and included death from cardiovascular disease, from coronary heart disease, or from any cause and nonfatal events of interest, including myocardial infarction and stroke.

Preliminary data on correlates of protection against HSV-1 are available. Antibody, but not cellular immunity, was correlated with protection against HSV-1. Among the HSV vaccinees tested in the immunogenicity cohort, 8 were subsequently infected by HSV-1 and 10 by HSV-2. Subjects with HSV-1 infection had significantly lower gD-2 ELISA antibody titers at month 7 (mean titer, 3561) than subjects who remained uninfected (mean titer, 6875; P=0.04). This was not the case for subjects with HSV-2 infection (mean titer, 6339; P=0.78). Cellular immune responses at month 2 or month 7 did not differ significantly between subjects who subsequently became infected with HSV-1 or HSV-2 and vaccinees who remained uninfected (see the Supplementary Appendix for details).

The efficacy of the gD-2 candidate vaccine against HSV-1 is important because epidemiologic studies suggest that sexual transmission of HSV-1 is increasing in the United States,1 although its prevalence among U.S. children is decreasing.11 Among control subjects in the present study, 60% of the cases of genital disease and two thirds of the infections (with or without disease) were caused by HSV-1. These data are similar to the finding that HSV-1 is the most common cause of genital herpes in college students and young heterosexual women, and similar trends are reported in other countries. HSV-1 now rivals HSV-2 as a cause of neonatal herpes disease. Public health officials and researchers will need to closely monitor seroprevalence trends as future herpes vaccines are developed and assessed.

Although the development of a vaccine that provides protection against HSV-1 genital disease is a substantial step forward, additional progress is needed before a herpes vaccine is likely to be approved for general use. Any candidate vaccine will probably have to have proven efficacy against both HSV-1 and HSV-2 disease. Prevention of infection (with or without disease) is also an important goal, because asymptomatic genital shedding of HSV may lead to the spread of the virus to newborns or sexual partners. This is a more difficult goal to achieve and may require approaches such as live attenuated vaccines or vaccine vectors to generate protection.

Solicited reports of adverse events included redness, swelling, and pain at the injection site, as well as fatigue, fever, headache, and malaise. The HSV vaccine was more reactogenic and was associated with local pain, redness, and swelling more often than was the control vaccine. There was a small but significant increase in systemic symptoms, including fatigue, fever, headache, and malaise, in the HSV-vaccine group (Table 3). Dose 2 and dose 3 of the HSV vaccine were not associated with increased reports of adverse events; in contrast, reactogenicity decreased slightly with additional vaccination.

Immunogenicity

The HSV vaccine was immunogenic and stimulated ELISA and neutralizing antibodies. As expected, control subjects did not have antibody to gD-2 on ELISA or neutralization of HSV-2. Geometric mean gD-2 ELISA titers were 21 at baseline and 6809 at month 7 after three doses of HSV vaccine; ELISA titers waned to 769 by month 20. HSV-2 neutralizing antibodies developed after two doses of HSV vaccine, but the median value fell to an undetectable level by study month 6 (see the Supplementary Appendix for details). After dose 3, HSV-2 neutralizing antibodies were again above the limit of detection (the mean titer at month 7 was 29) but fell to a median value that was undetectable by study month 16.

Discussion

Our findings of vaccine efficacy against HSV-1 and lack of efficacy against HSV-2 are puzzling in view of the previous two studies involving discordant couples that showed efficacy of this gD-2 vaccine against HSV-2.4 The difference in efficacy is likely to be due to some factor in the two populations studied. The distinguishing feature of discordant couples is that they are a highly selected group in which the uninfected partner is potentially repeatedly exposed to HSV by the infected partner. Attack rates of HSV-2 genital disease in the prior studies of gD-2 vaccine were high among uninfected women in discordant couples (13.9% for 19 months or 8.4% per year) and were reduced significantly by the vaccine (efficacy, 73% and 74% in the two trials; P=0.01 and P=0.02, respectively).4 Too few cases of HSV-1 genital disease occurred in women in the two previous studies to assess efficacy against HSV-1 (one case in each study among women who were seronegative at study entry).4 Potential reasons for vaccine efficacy in the discordant-couple population include selection bias for a population of women with relative resistance to HSV-2, with added benefits from a subunit vaccine; an undefined immunologic priming event from chronic sexual exposure to HSV-2 viral antigens from the infected partner; and less frequent sexual activity due to the long-term nature of the relationship as compared with sexual activity by couples in new relationships.

It is not apparent why the biologic characteristics of HSV-1 are different from those of HSV-2; the gD-2 vaccine induces significant protection against genital HSV-1 disease as well as HSV-1 infection, but not against disease or infection caused by HSV-2. Genital HSV-1 may be acquired primarily through oral–genital sex (although a history of oral sex was not a risk factor for HSV-1 acquisition in our study); a lower inoculum, an oral–genital route (possibly less traumatic sex), and a less suitable environment for HSV-1 replication are all possible explanations for protection by the vaccine against HSV-1 but not HSV-2. The gD-2 antigen is derived from HSV-2, but 89% amino acid homology is shared with gD-2 from HSV-1, which may explain the protection against HSV-1. Type-specific immune responses to vaccine antigen may reveal differences in antibody activity against HSV-1 and HSV-2. Whether HSV-1 is more easily neutralized by vaccine-induced antibodies must be determined by further laboratory studies.

Self-reported behaviors and demographic factors were analyzed for association with HSV-1 or HSV-2 infection in the per-protocol cohort for months 2 through 20. Analysis of self-reported behavioral risk factors was restricted to 5980 sexually active subjects. An increased risk of HSV-1 infection was associated with 6 or more lifetime sexual partners (hazard ratio, 2.2; 95% CI, 1.3 to 3.8) and more than 1 partner in the previous 12 months (hazard ratio, 1.9; 95% CI, 1.4 to 2.7). Subjects who were 23 years of age or older were less likely to acquire HSV-1 than 18-to-22-year-olds (hazard ratio for subjects 23 to 26 years of age, 0.6; 95% CI, 0.4 to 0.8; hazard ratio for subjects 27 to 30 years of age, 0.4; 95% CI, 0.3 to 0.8). Factors not associated with an increased risk of HSV-1 infection included race or ethnic group, country of residence (United States or Canada), having a current partner with herpes, ever having a partner with herpes, condom use, history of any sexually transmitted infection (STI), and oral sex.

An increased risk of HSV-2 infection was associated with having 6 or more lifetime sexual partners (hazard ratio, 2.0; 95% CI, 1.1 to 3.8), having 6 or more partners in the previous 12 months (hazard ratio, 2.7; 95% CI, 1.3 to 5.5), ever having a partner with herpes (hazard ratio, 3.0; 95% CI, 1.7 to 5.3), having a current partner with herpes (hazard ratio, 3.4; 95% CI, 1.8 to 6.4), a history of any STI (hazard ratio, 3.3; 95% CI, 2.2 to 5.0), nonwhite race (hazard ratio, 3.1; 95% CI, 2.1 to 4.6), and U.S. residence (hazard ratio, 2.7; 95% CI, 1.2 to 6.2). Factors not associated with increased risk of HSV-2 infection included age, ethnic group, condom use, and oral sex. Initiation of sexual activity after 15 years of age was associated with a decreased risk of both HSV-1 infection (hazard ratio for initiation at 16 to 18 years of age, 0.6; 95% CI, 0.4 to 0.8; hazard ratio after 18 years of age, 0.3; 95% CI, 0.2 to 0.6) and HSV-2 infection (hazard ratio for initiation at 16 to 18 years of age, 0.5; 95% CI, 0.3 to 0.8; hazard ratio after 18 years of age, 0.3; 95% CI, 0.2 to 0.6).

Genital Shedding of HSV-2

Forty-three subjects (30 in the HSV-vaccine group and 13 in the control group) with HSV-2 infection collected anogenital swabs on 60 consecutive days, beginning 3 to 6 months after disease onset (15 subjects in the HSV-vaccine group and 9 in the control group) or seroconversion (15 subjects in the HSV-vaccine group and 4 in the control group). Analysis of these swabs showed that the rate of viral shedding was higher among the HSV-vaccine recipients than among controls (29% vs. 19%; relative risk, 1.55; 95% CI, 1.28 to 1.86). The mean quantity of HSV DNA on days with shedding did not differ between the two groups.

Statistical Analysis

The trial was designed to have 80% power to detect a vaccine efficacy of 75% with 45% as the lower limit of the 95% confidence interval. It met the information goal, observing 70 of a planned 72 cases of genital herpes disease in the per-protocol cohort. The trial was monitored by an independent data safety and monitoring board sponsored by the National Institute of Allergy and Infectious Diseases, which met quarterly and reviewed the study for safety. At a prespecified interim analysis, the board also reviewed the trial for futility. The sample size was extended once in response to higher-than-anticipated attrition. Vaccine efficacy was estimated as 1 minus the relative risk from a Cox proportional-hazards model fit to the time to first acquisition of each study end point. Rates of loss-to-follow-up were similar between the two study groups, and noninformative censoring was assumed. A post hoc assessment of demographic and behavioral risk factors for HSV acquisition was performed with the use of a Cox proportional-hazards model adjusted for the receipt of HSV vaccine. All reported P values are two-tailed and have not been adjusted for multiple testing. The per-protocol and intention-to-treat cohorts are defined in the legend for Figure 1.
Results
Characteristics of the Study Population

Fifty clinical sites in the United States and Canada screened a total of 31,770 women for antibodies to HSV-1 and HSV-2; 12,468 women were seronegative for both HSV-1 and HSV-2, of whom 8323 met the other eligibility criteria and were enrolled between January 14, 2003, and November 19, 2007.

Vaccine Efficacy

In the control group, HSV-1 was a more common cause of genital disease than HSV-2 (21 cases caused by HSV-1 vs. 14 cases caused by HSV-2). Efficacy against genital disease caused by HSV-1 was observed (vaccine efficacy, 58%; 95% CI, 12 to 80) (Figure 2B), but efficacy was not observed against HSV-2 disease (−38%; 95% CI, −167 to 29) (Figure 2C). Three doses of vaccine were associated with efficacy against HSV-1 (77%; 95% CI, 31 to 92) but not HSV-2 (−40%; 95% CI, −234 to 41). An analysis in which the case definition was limited to culture-positive cases (excluding HSV cases diagnosed according to clinical and serologic criteria) also showed efficacy against HSV-1 (two-dose efficacy, 69%; 95% CI, 25 to 87; three-dose efficacy, 82%; 95% CI, 35 to 95).

The HSV vaccine provided protection against infection caused by HSV-1 or HSV-2 (efficacy, 22%; 95% CI, 2 to 38). This overall finding of protection against infection was driven by efficacy against HSV-1 infection (35%; 95% CI, 13 to 52), whereas efficacy against HSV-2 infection was not observed (−8%; 95% CI, −59 to 26).

The control vaccine, inactivated hepatitis A vaccine (Havrix, GlaxoSmithKline), was formulated as 720 enzyme-linked immunosorbent assay (ELISA) units of inactivated hepatitis A virus combined with 0.5 mg of alum, in a volume of 0.5 ml. For the study to be blinded, the control vaccine was given at 0, 1, and 6 months in doses containing one half the usual volume and one half the usual amount of antigen.

Study Design

The double-blind, randomized field trial was designed in collaboration among the trial sponsors, the National Institutes of Health (NIH) and GlaxoSmithKline; the study chair; the executive committee; and the scientific leadership group. Data were collected with the use of the GlaxoSmithKline remote data-entry system and were monitored by GlaxoSmithKline. All the authors and the trial sponsors vouch for the accuracy and completeness of the data. Data were electronically transferred to EMMES, a contract research organization, where they were analyzed according to the analysis plan prepared by biostatisticians at GlaxoSmithKline and EMMES, with input to the analysis plan from the NIH, the study chair, and the executive committee. The manuscript was drafted by the first author, with input from the biostatisticians at EMMES and from the executive committee.

Study End Points

The primary end point of the study was prevention of genital herpes disease caused by HSV-1, HSV-2, or both from month 2 (1 month after vaccine dose 2) through month 20. Genital disease was defined as clinically compatible signs and symptoms confirmed by viral culture, seroconversion, or both within 6 months after disease onset. Secondary end points included prevention of HSV-1 or HSV-2 infection (with or without disease) from month 2 through month 20 (two-dose efficacy) or month 7 through month 20 (three-dose efficacy) and prevention of genital herpes disease caused by individual HSV types. Cases of infection and disease were determined centrally by an independent, blinded end-point review committee with the use of documented criteria.

Substudy of Viral Shedding

Subjects identified as having acquired genital HSV-2 disease or HSV-2 infection during the study were invited to participate in an evaluation of viral shedding. Subjects were instructed to collect daily swabs from the anogenital area for 60 consecutive days and to maintain a diary of genital signs and symptoms, as previously described, beginning 3 to 6 months after HSV-2 seroconversion or disease onset.

Laboratory Studies

Western blot analysis (University of Washington Clinical Virology Laboratory at Seattle Children’s Hospital) was used to confirm HSV-1– or HSV-2–seronegative status at study entry and seroconversion during the follow-up period.6 Seroconversion to HSV-1 or HSV-2 was defined as a positive Western blot analysis in a subject with a previously negative analysis for the corresponding HSV type.

Serum specimens from a random subset of 611 subjects in the HSV-vaccine group and 223 subjects in the control group were assessed for the development of antibodies to vaccine antigens with the use of ELISA4,7 for gD-2 and virus neutralization of HSV-2 at 0, 2, 6, 7, 12, 16, and 20 months. Long-term genital shedding of HSV-2 DNA was assessed with the use of a quantitative, real-time, fluorescence-based polymerase-chain-reaction assay, as described previously, with a positive result defined as 150 copies per milliliter.

The fourth and final habit is self-study. Beyond ensuring that their clinical practices are consistent with the most recent science, these organizations also examine positive and negative deviance in their own care and outcomes, seeking new insights and better outcomes for their patients.5 By contrast, most health care organizations treat clinical knowledge as a property of the individual clinician, “managing” knowledge only by hiring and credentialing competent professional staff.

High-value organizations treat clinical knowledge as an organizational as well as individual property. They create knowledge and innovations with the use of some common tools (sentinel-event reporting and root-cause analysis) and some less common ones (monitoring of protocol overrides and rapid-cycle experimentation). Some have units — for instance, the Mayo Clinic’s See-Plan-Act-Refine-Communicate (SPARC) program — that are dedicated to developing innovations in-house, and most have academies to teach leaders and staff the principles and techniques for improving the value of care and to support the application of these principles to high-priority clinical programs and processes. Most important, these organizations deliberately nurture a culture that supports learning by encouraging dissenting views and overriding of specified clinical decision rules (habit 1).

These habits are not unique to high-value health care organizations. Many delivery organizations engage in some of them — designing clinical pathways and reporting on quality and safety, for instance. But high-value organizations are distinct in two important ways. First, they engage in all four habits systematically. For them, these activities are truly habits, baked into their structures, culture, and routines, not simply short-lived projects. Second, the habits are integrated into a comprehensive system for clinical management that is focused more on clinical processes and outcomes than on resources. A consensus is emerging about how to manage clinical care.

Each organization expresses these four habits differently. Each faces a unique regulatory and reimbursement environment and has different resources, so each uses different tools and terminologies, varying in the details of how they specify decisions or measure clinical processes. Still, the habits are the same. As we seek models for achieving high-value health care, we must look past the particularities of local structures and tactics to the habits they reflect. Although a “dominant” delivery model may not be transferrable, the habits of high-value health care may be.

The specification of choices, transitions, subgroups, and patient pathways represents a substantial investment in advance planning. It contrasts sharply with the common practice of focusing management planning on the utilization of expensive resources, such as tests, procedures, and bed-days, rather than on the problems these resources are designed to solve. Many hospitals and clinicians do not plan care processes in advance in such detail; instead, they treat each new patient or problem as a random draw from a heterogeneous population and must therefore reinvent the strategy for solving it.

A second common habit is infrastructure design. High-value health care organizations deliberately design microsystems3 — including staff, information and clinical technology, physical space, business processes, and policies and procedures that support patient care — to match their defined subpopulations and pathways. Thus, different conditions or patient groups have different microsystem designs. The various tasks of care are allocated to different members of a clinical team (including the patient), with the skill and training of each staff member matched to the work. Such organizations make thoughtful use of assistive personnel and alternative providers, and they ensure that each has the necessary resources by carefully designing the supply chain of equipment and information, simplifying workflow, and reducing work stress. They also harmonize the parts of their management system so that budgets, incentives, data, goals, clinical processes, educational programs, and team structures are all mutually reinforcing.4 Unit-level routines, such as joint ward rounds, team meetings, and executive “walk-arounds,” help tie microsystem components together.

Attention to microsystem design and integration represents an important shift away from general-services-organization designs that use a single platform to meet the needs of many different patient groups and that focus on maximizing the use of scarce resources, such as operating-room slots, ICU beds, and physicians.

The third habit is measurement and oversight. For many, measurement of clinical operations is driven by external audiences: payers, regulators, and rating agencies. Although high-value organizations share this reporting obligation, they primarily use measurement for internal process control and performance management. They collect more (and more detailed) measurements than those required for external reporting, selecting those that inform staff about clinical performance. For instance, of the 200-plus measurements used by Intermountain, more than two thirds were developed or refined internally rather than imported unmodified from external agencies. Moreover, such organizations integrate their measurement activities with other organizational priorities such as pay for performance, annual target setting, and improvement activities, making measurement an integral part of accountability and performance management. For example, each year Intermountain’s board selects a different group of measurements from the institution’s overall measurement set to use for annual quality and efficiency bonuses.