Results of a Remotely Delivered Hypertension and Lipid Program in More Than 10 000 Patients Across a Diverse Health Care Network.

Importance: Blood pressure (BP) and cholesterol control remain challenging. Remote care can deliver more effective care outside of traditional clinician-patient settings but scaling and ensuring access to care among diverse populations remains elusive. Objective: To implement and evaluate a remote hypertension and cholesterol management program across a diverse health care network. Design, Setting, and Participants: Between January 2018 and July 2021, 20 454 patients in a large integrated health network were screened; 18 444 were approached, and 10 803 were enrolled in a comprehensive remote hypertension and cholesterol program (3658 patients with hypertension, 8103 patients with cholesterol, and 958 patients with both). A total of 1266 patients requested education only without medication titration. Enrolled patients received education, home BP device integration, and medication titration. Nonlicensed navigators and pharmacists, supported by cardiovascular clinicians, coordinated care using standardized algorithms, task management and automation software, and omnichannel communication. BP and laboratory test results were actively monitored. Main Outcomes and Measures: Changes in BP and low-density lipoprotein cholesterol (LDL-C). Results: The mean (SD) age among 10 803 patients was 65 (11.4) years; 6009 participants (56%) were female; 1321 (12%) identified as Black, 1190 (11%) as Hispanic, 7758 (72%) as White, and 1727 (16%) as another or multiple races (including American Indian or Alaska Native, Asian, Native Hawaiian or Other Pacific Islander, unknown, other, and declined to respond; consolidated owing to small numbers); and 142 (11%) reported a preferred language other than English. A total of 424 482 BP readings and 139 263 laboratory reports were collected. In the hypertension program, the mean (SD) office BP prior to enrollment was 150/83 (18/10) mm Hg, and the mean (SD) home BP was 145/83 (20/12) mm Hg. For those engaged in remote medication management, the mean (SD) clinic BP 6 and 12 months after enrollment decreased by 8.7/3.8 (21.4/12.4) and 9.7/5.2 (22.2/12.6) mm Hg, respectively. In the education-only cohort, BP changed by a mean (SD) -1.5/-0.7 (23.0/11.1) and by +0.2/-1.9 (30.3/11.2) mm Hg, respectively (P < .001 for between cohort difference). In the lipids program, patients in remote medication management experienced a reduction in LDL-C by a mean (SD) 35.4 (43.1) and 37.5 (43.9) mg/dL at 6 and 12 months, respectively, while the education-only cohort experienced a mean (SD) reduction in LDL-C of 9.3 (34.3) and 10.2 (35.5) mg/dL at 6 and 12 months, respectively (P < .001). Similar rates of enrollment and reductions in BP and lipids were observed across different racial, ethnic, and primary language groups. Conclusions and Relevance: The results of this study indicate that a standardized remote BP and cholesterol management program may help optimize guideline-directed therapy at scale, reduce cardiovascular risk, and minimize the need for in-person visits among diverse populations.

Heart rate, beta-blocker use, and outcomes of heart failure with reduced ejection fraction.

Aims: High resting heart rate (HR ≥70 b.p.m.) is associated with worse clinical outcomes in heart failure with reduced ejection fraction (HFrEF). Heart rate, guideline-directed medical therapy (GDMT) with beta-blocker (BB), and cardiovascular outcomes were evaluated in a large integrated health network. Methods and results: Using electronic health records we examined patients with chronic HFrEF (ejection fraction ≤35%) in sinus rhythm with at least 1 year of follow-up and available serial HR and medication data between 1 January 2000 and 31 December 2014. Among 6071 patients followed for median of 1330 days across 73 586 total visits, median HR remained stable over time with 61.2% of the follow-up period with HR ≥70 b.p.m. At baseline, 27.9% of patients were on ≥ 50% GDMT target BB dose, 16.2% subjects at baseline, and 19.4% at the end of follow-up had HR ≥70 b.p.m. despite receiving ≥50% of target BB dose. In adjusted analyses, baseline HR was associated with all-cause mortality/heart failure (HF) hospitalization (hazard ratio 1.28 per 15 b.p.m. Heart rate increase; P < 0.001). In comparison, hazard ratio for BB dose was 0.97 (per 77.2 mg increase; P = 0.36). When evaluating patients based on HR and BB dose there was a significant difference in the cumulative hazard for all-cause mortality or HF hospitalization (P < 0.001). For HF hospitalization, hazard appeared to be more closely associated with HR rather than BB dose (P = 0.01). Conclusion: In a real-world analysis, high resting HR was common in HFrEF patients and associated with adverse outcomes. Opportunities exist to improve GDMT and achieve HR control.

Proton-Pump Inhibitors Reduce Gastrointestinal Events Regardless of Aspirin Dose in Patients Requiring Dual Antiplatelet Therapy.

BACKGROUND: The COGENT (Clopidogrel and the Optimization of Gastrointestinal Events Trial) showed that proton-pump inhibitors (PPIs) safely reduced rates of gastrointestinal (GI) events in patients requiring dual antiplatelet therapy (DAPT). However, utilization of appropriate prophylactic PPI therapy remains suboptimal, especially with low-dose aspirin. OBJECTIVES: The authors investigated the safety and efficacy of PPI therapy in patients receiving DAPT in low- and high-dose aspirin subsets. METHODS: Randomized patients with available aspirin dosing information in COGENT (N = 3,752) were divided into "low-dose" (≤ 100 mg) and "high-dose" (>100 mg) aspirin groups. The primary GI and cardiovascular endpoints were composite upper GI events and major adverse cardiac events, respectively. All events were adjudicated by independent, blinded gastroenterologists and cardiologists. RESULTS: Median duration of follow-up was 110 days. Low-dose aspirin users (n = 2,480; 66.1%) were more likely to be older, female, and have higher rates of peripheral artery disease, prior stroke, and hypertension, whereas high-dose aspirin users (n = 1,272; 33.9%) had higher rates of hyperlipidemia, smoking, a history of percutaneous coronary intervention, and were more than twice as likely to be enrolled from sites within the United States (80.4% vs. 39.8%). High-dose aspirin was associated with similar 180-day Kaplan-Meier estimates of adjudicated composite GI events (1.7% vs. 2.1%; adjusted hazard ratio: 0.88; 95% confidence interval: 0.46 to 1.66) and major adverse cardiac events (4.8% vs. 5.5%; adjusted hazard ratio: 0.73; 95% confidence interval: 0.48 to 1.11) compared with low-dose aspirin. Randomization to PPI therapy reduced 180-day Kaplan-Meier estimates of the primary GI endpoint in low-dose (1.2% vs. 3.1%) and high-dose aspirin subsets (0.9% vs. 2.6%; p for interaction = 0.80), and did not adversely affect the primary cardiovascular endpoint in either group. CONCLUSIONS: Gastroprotection with PPI therapy should be utilized in appropriately selected patients with coronary artery disease requiring DAPT, even if the patients are on low-dose aspirin. (Clopidogrel and the Optimization of Gastrointestinal Events Trial [COGENT]; NCT00557921).

Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE): updated standing orders for ST-segment elevation myocardial infarction and unstable angina/non-ST-segment elevation myocardial infarction.

The Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) acute coronary syndromes critical pathway toolkit has been updated based on the 2009 focused updates of the American College of Cardiology/American Heart Association guidelines for the management of patients with ST-segment elevation myocardial infarction (STEMI) and American College of Cardiology/American Heart Association/Society for Cardiovascular Angiography and Interventions guidelines on percutaneous coronary intervention (PCI). This review highlights the major changes cited in the focused updates, which have been incorporated into the STRIVE standing orders for STEMI and unstable angina/non-ST-segment elevation myocardial infarction (UA/NSTEMI). The updated STEMI and UA/NSTEMI standing orders and other tools are available to clinicians online on the STRIVE Web site.

Effect of intensive statin therapy on clinical outcomes among patients undergoing percutaneous coronary intervention for acute coronary syndrome. PCI-PROVE IT: A PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) Substudy.

OBJECTIVES: The goal of this analysis was to determine whether intensive statin therapy, compared with moderate-dose statin therapy, leads to a reduction in major adverse cardiovascular events (MACE) among patients undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS). BACKGROUND: When compared with moderate-dose statins, intensive statin therapy reduces MACE among patients with ACS. The role of intensive statin therapy specifically among patients who undergo PCI for ACS is unknown. METHODS: Outcomes were compared in 2,868 patients who underwent PCI for ACS just prior to enrollment in the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial, which randomized patients to either atorvastatin 80 mg or pravastatin 40 mg daily. The incidence of the primary composite end point of all-cause mortality, myocardial infarction, unstable angina leading to hospitalization, and revascularization after 30 days and stroke was evaluated, as was the incidence of target vessel revascularization (TVR) and non-TVR during follow-up. RESULTS: Treatment with 80 mg atorvastatin reduced the incidence of the composite end point (21.5% vs. 26.5%, hazard ratio: 0.78, 95% confidence interval: 0.67 to 0.91, p=0.002) and lowered the incidence of both TVR (11.4% vs. 15.4%, p=0.001) and non-TVR (8.0% vs. 10.5%, p=0.017) compared with 40 mg pravastatin. After adjusting for on-treatment serum low-density lipoprotein cholesterol and C-reactive protein concentrations, the odds of TVR with high-dose statin therapy remained significant (odds ratio: 0.74, p=0.015) while the odds of non-TVR did not (odds ratio: 0.92, p=0.55). CONCLUSIONS: Among patients with ACS who undergo PCI, intensive statin therapy reduces MACE compared with moderate-dose statin therapy. The reduction in the incidence of TVR was independent of low-density lipoprotein cholesterol and C-reactive protein lowering and may therefore be due, at least in part, to a pleiotropic effect of high-dose statin therapy. (PROVE IT-TIMI 22; NCT00382460).

Reduction in recurrent cardiovascular events with intensive lipid-lowering statin therapy compared with moderate lipid-lowering statin therapy after acute coronary syndromes from the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial.

OBJECTIVES: In addition to reducing first events in patients after an acute coronary syndrome (ACS), we hypothesized that high-dose atorvastatin 80 mg would also reduce recurrent cardiovascular events, and therefore total events, compared with pravastatin 40 mg during the 2-year follow-up. BACKGROUND: In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22) trial, more intensive lipid lowering with high-dose atorvastatin reduced the first occurrence of the primary end point (death, myocardial infarction, unstable angina requiring rehospitalization, stroke, or revascularization > or = 30 days) compared with moderate lipid lowering with pravastatin. METHODS: Poisson regression analysis was performed to compare the number of occurrences of the primary end point between high-dose atorvastatin and pravastatin in the PROVE IT-TIMI 22 trial. RESULTS: As previously reported, first primary end point events were reduced by 16% with atorvastatin 80 mg versus pravastatin 40 mg (n = 464 vs. n = 537, respectively; p = 0.005). Additional events were also reduced by 19% with atorvastatin 80 mg (n = 275 vs. n = 340, respectively; p = 0.009). Overall, there were 138 fewer primary efficacy events with atorvastatin 80 mg versus pravastatin 40 mg (n = 739 vs. n = 877, respectively; rate ratio: 0.85, 95% confidence interval: 0.77 to 0.94, p = 0.001). CONCLUSIONS: Although analytic techniques commonly used in clinical outcomes trials censor patients who experience a component of the primary composite end point, total cardiovascular events are important to patients, clinicians, and health care payers. Maintaining low levels of low-density lipoprotein cholesterol is central to preventing additional atherosclerotic development and subsequent cardiovascular events. Atorvastatin 80 mg, a more intensive low-density lipoprotein cholesterol lowering agent, reduced both first and subsequent primary end point events compared with pravastatin 40 mg after ACS.

Updated Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) ST-segment elevation myocardial infarction critical pathway toolkit.

The Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) acute coronary syndromes critical pathway toolkit has been revised again based on the 2007 focused update of the American College of Cardiology/American Heart (ACC/AHA) Association guidelines for the management of patients with ST-segment elevation myocardial infarction (STEMI). A previous update of the toolkit incorporated the 2007 ACC/AHA guidelines for unstable angina/non-ST-segment elevation myocardial infarction. This review highlights the major revisions to the STEMI guidelines, and illustrates and describes the revised STRIVE critical pathway tools for STEMI, which include pathway flowcharts, standing orders, pocket cards, and posters. The updated STEMI tools are available to clinicians online on the STRIVE Website.

Updated Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) unstable angina/non-ST elevation myocardial infarction critical pathway toolkit.

The Strategies and Therapies for Reducing Ischemic and Vascular Events (STRIVE) acute coronary syndromes (ACS) critical pathway toolkit, developed in 2002, has been revised and updated. The updated toolkit is based on the American College of Cardiology/American Heart Association 2007 guidelines for the management of patients with unstable angina/non-ST-segment elevation myocardial infarction (UA/NSTEMI). This review highlights the major revisions to the UA/NSTEMI guidelines and illustrates and describes the revised STRIVE critical pathway tools, which include pathway flowcharts, standing orders, pocket cards, posters, and form letters. These materials are being made available online to help physicians, nurses, and hospitals implement the new guidelines and thus improve the quality of care and outcomes for patients with ACS.

High-dose atorvastatin does not negatively influence clinical outcomes among clopidogrel treated acute coronary syndrome patients--a Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) analysis.

BACKGROUND: Clopidogrel is inactive in vitro and is metabolized by hepatic cytochrome P-450-3A4 to produce active metabolites. Unlike pravastatin, atorvastatin is a statin that is subject to metabolism by cytochrome P-450-3A4, and drug-drug interactions with other potent inhibitors of this cytochrome system have been demonstrated. However, the clinical impact of this interaction has created debate. METHODS: In the PROVE IT-TIMI 22 study, 4162 patients with an acute coronary syndrome within the preceding 10 days were randomly assigned in a 1:1 fashion to pravastatin 40 mg or atorvastatin 80 mg daily. The primary efficacy outcome measure was the time from randomization until the first occurrence of a component of the primary end point: death from any cause, myocardial infarction, documented unstable angina requiring rehospitalization, revascularization with either percutaneous coronary intervention or coronary artery bypass grafting, or stroke. RESULTS: At 30 days, there was a trend for less occurrence of the primary end point in patients randomized to atorvastatin compared with pravastatin, irrespective of whether they were taking clopidogrel. This becomes significant at 2-year follow-up in clopidogrel-treated patients (21.66 % vs 26.18% P = .0091). There was no evidence of interaction in the clopidogrel/no clopidogrel subgroup for the primary end point (interaction P = .65) or the components of the composite. CONCLUSION: In conclusion, the beneficial affects of atorvastatin 80 mg in reducing the primary end point at 2 years is independent of coadministration with clopidogrel.

Effect of intensive lipid-lowering therapy on mortality after acute coronary syndrome (a patient-level analysis of the Aggrastat to Zocor and Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 trials).

Compared with moderate lipid lowering with standard-dose statin therapy, intensive lipid lowering with high-dose statin therapy after acute coronary syndromes (ACS) significantly reduces cardiovascular events. However, the 2 trials of high-dose versus standard-dose statin therapy in patients with ACS, Aggrastat to Zocor (A to Z) and Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 (PROVE-IT-TIMI 22), were not individually powered to evaluate the impact on mortality alone. In this study, a pooled, patient-level analysis of these trials of 8,658 post-ACS patients was performed to provide a more robust estimate of the impact of intensive statin therapy on mortality. By 8 months, achieved low-density lipoprotein levels were lower in the group with intensive statin therapy (median 64 mg/dl, interquartile range 51 to 81) than in the group with moderate statin therapy (median 87 mg/dl, interquartile range 71 to 107) (p <0.001). All-cause mortality was significantly reduced in the group with intensive statin therapy compared with the group with moderate statin therapy (3.6% vs 4.9%, hazard ratio 0.77, 95% confidence interval 0.63 to 0.95, p = 0.015), without significant interaction by trial (interaction p = 0.63). The reduction in all-cause mortality with intensive statin therapy was consistent across key subgroups. In conclusion, in this analysis of >8,600 patients, intensive lipid lowering with high-dose statin therapy after ACS was associated with reduced mortality compared with moderate lipid lowering with standard-dose statin therapy. On the basis of these findings, 1 death was prevented for every 95 patients treated with high-dose statin therapy for 2 years. The results of this pooled analysis provide further evidence for early intensive statin therapy after ACS.

Long-term prognostic value of neopterin: a novel marker of monocyte activation in patients with acute coronary syndrome.

BACKGROUND: Monocyte activation is believed to play an important role in the pathogenesis of acute coronary syndromes (ACS). Neopterin is a soluble marker of monocyte activation, and elevated levels are of prognostic value in patients with stable coronary artery disease. METHODS AND RESULTS: Neopterin levels were measured on average at 7 days (in 3946 patients) and at 4 months (in 3369 patients) after ACS in the PRavastatin Or atorVastatin Evaluation Infection Therapy-Thrombolysis In Myocardial Infarction (PROVE IT-TIMI 22) trial. We assessed the relationship between plasma neopterin levels and the risk of death and death or acute coronary events (nonfatal myocardial infarction or unstable angina) over 2 years. Seven days after an ACS event, neopterin levels > or = 12.11 nmol/L (upper quartile, derived from a post hoc analysis) were associated with an increased risk of death and an increased risk of death or acute coronary events after adjustment for age, gender, history of diabetes mellitus, history of hypertension, history of smoking, type of ACS presentation, use of percutaneous coronary intervention for the index event, statin regimen, low-density lipoprotein cholesterol, and high-sensitivity C-reactive protein (hazard ratio, 1.86 [95% CI, 1.24 to 2.77], P=0.003; and hazard ratio, 1.33 [95% CI, 1.09 to 1.63] P=0.006, respectively). Neopterin levels > or = 12.11 nmol/L at 4 months remained a predictor of death alone and of death or acute coronary events after multivariable adjustment that included adjustment for month 4 low-density lipoprotein cholesterol, high-sensitivity C-reactive protein, and statin regimen (hazard ratio, 2.39 [95% CI, 1.43 to 3.99], P=0.001; and hazard ratio, 1.60 [95% CI, 1.21 to 2.11], P=0.001). High-dose atorvastatin significantly attenuated the risk among subjects with neopterin levels > or = 12.11 nmol/L at baseline (interaction P for death or acute coronary event, 0.018). CONCLUSIONS: Increased monocyte activation detected by an elevated plasma neopterin level identifies patients at long-term risk of death or recurrent acute coronary events after ACS. Intensive statin therapy significantly attenuates the risk of recurrent events among patients with an elevated neopterin level.

Lipoprotein-associated phospholipase A2 and its association with cardiovascular outcomes in patients with acute coronary syndromes in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is associated with the risk of cardiovascular (CV) events in population-based studies. The prognostic value of Lp-PLA2 in patients with acute coronary syndromes (ACS) has not been established. METHODS AND RESULTS: Plasma levels of Lp-PLA2 activity were measured at baseline (n=3648) and 30 days (n=3265) in patients randomized to atorvastatin 80 mg/d or pravastatin 40 mg/d after ACS in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction) trial. The primary end point was death, myocardial infarction, unstable angina, revascularization, or stroke (mean follow-up 24 months). At baseline after ACS, the risk of recurrent CV events was similar across all quintiles of Lp-PLA2 activity (Ptrend=0.88). Overall, mean levels of Lp-PLA2 were lower at 30 days of follow-up than at baseline (35.7 versus 40.9 nmol.min(-1).mL(-1), P<0.001). In particular, treatment with atorvastatin 80 mg/d was associated with a 20% reduction in Lp-PLA2 activity (P<0.001), whereas Lp-PLA2 rose 3.6% with pravastatin 40 mg/d (P<0.001). Patients with 30-day Lp-PLA2 activity in the highest quintile were at significantly increased risk of recurrent CV events compared with those in the lowest quintile (26.4% versus 17.6%, Ptrend=0.002). After adjustment for cardiac risk factors, treatments, achieved low-density lipoprotein (LDL), and C-reactive protein, Lp-PLA2 activity in the highest quintile remained independently associated with a higher risk of recurrent CV events (adjusted hazard ratio 1.33, 95% confidence interval [CI] 1.01 to 1.74). CONCLUSIONS: Lp-PLA2 is not useful for risk stratification when measured early after ACS. At 30 days, Lp-PLA2 activity is significantly lowered with high-dose statin therapy and is associated with an increased risk of CV events independent of C-reactive protein and LDL cholesterol levels.

Early and late benefits of high-dose atorvastatin in patients with acute coronary syndromes: results from the PROVE IT-TIMI 22 trial.

OBJECTIVES: Our objective was to determine the timing of benefit with intensive statin therapy after an acute coronary syndrome (ACS) in two time windows: an early window soon after an ACS and a late window in more stable patients. BACKGROUND: The Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis In Myocardial Infarction 22 (PROVE IT-TIMI 22) trial showed that the use of intensive statin therapy improved clinical outcomes over two years in ACS patients versus standard therapy. The relative contributions of early or late effects to the overall clinical efficacy of intensive therapy are presently unclear. METHODS: A total of 4,162 patients with ACS were recruited in the PROVE IT-TIMI 22 trial. Patients were randomized to intensive statin therapy (atorvastatin, 80 mg) or standard therapy (pravastatin, 40 mg). The composite triple end point of death, MI, or rehospitalization for recurrent ACS was determined in each group at 30 days. The composite triple and primary end points were assessed in stable patients from six months to the end of study, after censoring for clinical events before six months. RESULTS: The composite end point at 30 days occurred in 3.0% of patients receiving atorvastatin 80 mg versus 4.2% of patients receiving pravastatin 40 mg (hazard ratio [HR] = 0.72; 95% confidence interval [CI], 0.52 to 0.99; p = 0.046). In stable patients, atorvastatin 80 mg was associated with a composite event rate of 9.6% versus 13.1% in the pravastatin 40 mg group (HR = 0.72; 95% CI, 0.58 to 0.89; p = 0.003). CONCLUSIONS: Intensive statin therapy early after ACS leads to a reduction in clinical events at 30 days, consistent with greater early pleiotropic effects. In stable patients, intensive statin therapy provides long-term reduction in clinical events when compared with standard therapy. Thus, ACS patients should be started in-hospital and continued long-term on intensive statin therapy.

Atorvastatin and cardiovascular protection: a review and comparison of recent clinical trials.

Until recently, atorvastatin was known only as a new but more potent statin ('me too' drug) for lowering low-density lipoprotein cholesterol. In the last 2 years, data has become available on nearly 32,000 patients, in clinical settings ranging from primary prevention to acute coronary syndromes. These trials show the remarkably consistent clinical benefit of atorvastatin in patients with hypertension, diabetes, acute coronary syndromes, stable coronary disease with reductions in death, myocardial infarction and stroke, as well as in prevention of atherosclerosis progression. In addition, new data are also emerging to suggest that intensive therapy with high dose atorvastatin 80 mg is associated with a greater reduction in inflammatory markers, such as C-reactive protein, compared with other statin regimens. This suggests that intensive therapy with atorvastatin is associated with a potent pleiotropic effect. This review aims to summarise the recently concluded and ongoing clinical trials and to stimulate further reading.

Intensive versus moderate lipid lowering with statins after acute coronary syndromes.

BACKGROUND: Lipid-lowering therapy with statins reduces the risk of cardiovascular events, but the optimal level of low-density lipoprotein (LDL) cholesterol is unclear. METHODS: We enrolled 4162 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and compared 40 mg of pravastatin daily (standard therapy) with 80 mg of atorvastatin daily (intensive therapy). The primary end point was a composite of death from any cause, myocardial infarction, documented unstable angina requiring rehospitalization, revascularization (performed at least 30 days after randomization), and stroke. The study was designed to establish the noninferiority of pravastatin as compared with atorvastatin with respect to the time to an end-point event. Follow-up lasted 18 to 36 months (mean, 24). RESULTS: The median LDL cholesterol level achieved during treatment was 95 mg per deciliter (2.46 mmol per liter) in the standard-dose pravastatin group and 62 mg per deciliter (1.60 mmol per liter) in the high-dose atorvastatin group (P<0.001). Kaplan-Meier estimates of the rates of the primary end point at two years were 26.3 percent in the pravastatin group and 22.4 percent in the atorvastatin group, reflecting a 16 percent reduction in the hazard ratio in favor of atorvastatin (P=0.005; 95 percent confidence interval, 5 to 26 percent). The study did not meet the prespecified criterion for equivalence but did identify the superiority of the more intensive regimen. CONCLUSIONS: Among patients who have recently had an acute coronary syndrome, an intensive lipid-lowering statin regimen provides greater protection against death or major cardiovascular events than does a standard regimen. These findings indicate that such patients benefit from early and continued lowering of LDL cholesterol to levels substantially below current target levels.

Treatment algorithms and critical pathways for acute coronary syndromes.

Although numerous clinical trials have identified many advances in the treatment of patients with acute coronary syndromes (ACS), registries of clinical practice have identified that in clinical practice a large proportion of patients do not receive guideline-recommended therapies. In addition to development and dissemination of national guidelines, there is a need for specific tools to ensure that the guideline recommendations are implemented on a patient-by-patient basis. Better adherence to practice guidelines has been found to be associated with improved outcomes. Critical pathways and/or the process of Continuous Quality Improvement (CQI) are means of trying to improve care. Critical pathways are standardized protocols that aim to optimize and streamline patient care, which usually involve standardized order sets, (or computerized ones), and/or simple pocket cards, reminders, or checklists of the appropriate therapies. Another key part of an overall CQI effort is to monitor data on performance-i.e. utilization of guideline recommended therapies. Several well-conducted studies, showing that particular use of critical pathways, can lead to improve quality of care.