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Given the complex clinical circumstances of out-of-hospital cardiac arrest, precise control of the time to the first analysis of cardiac rhythm is difficult to achieve. In our trial, the duration of CPR before the first analysis of rhythm did not fall within the assigned target for 36% of the patients. Although this observation raises the question of quality control in training and trial supervision, the participating EMS agencies were high-functioning services with advanced-level paramedics; in addition, they had collected high-quality patient data before the start of the trial, and they made continuous efforts to reinforce performance targets. Thus, although implementation of the protocol was imperfect, it nonetheless represents the degree of precision with which such therapies are likely to be practiced in the clinical setting of out-of-hospital cardiac arrest. Furthermore, despite this limitation, there was very good separation between the two study groups in the duration of CPR, and a variety of data analyses confirmed the primary finding of no significant difference in the outcome between patients who had early rhythm analysis and those who had later rhythm analysis.

Our results indicate that in most cases, the outcome is similar with as few as 30 seconds and as many as 180 seconds of EMS-administered CPR before the analysis of cardiac rhythm. The exception is the case of cardiac arrest witnessed by EMS responders, which was not evaluated in this study and for which rapid defibrillation remains the standard of care.13 Our results also do not address the strategy of immediate analysis of cardiac rhythm without any preceding CPR, since we deliberately insisted on some CPR for the early-analysis group, in the belief that good patient care required cardiopulmonary support while the defibrillator was being prepared.

Exploratory examination of our data suggests that a strategy of brief CPR and early analysis may be more appropriate than longer CPR and later analysis for patients who have received CPR from a bystander before the arrival of professional responders. Conversely, for patients who have not received CPR from a bystander, there is no approach that is clearly advantageous with respect to the time to analysis of rhythm. The 2010 guidelines of the AHA–ILCOR give little direction as to the preferred period of CPR before analysis of cardiac rhythm. Each EMS system should consider its operational situation when deciding on its strategy for initial EMS-administered CPR. We believe that it is important to administer CPR for some period while the defibrillator pads are being applied and that compressions should be of high quality with minimal interruptions.

In conclusion, in a large clinical trial, we evaluated the timing of the analysis of cardiac rhythm during CPR in patients who had an out-of-hospital cardiac arrest that was not witnessed by EMS personnel. We found no difference in the outcome between the EMS strategy of a brief period of CPR before early rhythm analysis and that of a longer period of CPR before delayed rhythm analysis.

In this randomized trial, we tested the hypothesis that patients with an out-of-hospital cardiac arrest might benefit from the administration of CPR by EMS personnel for approximately 3 minutes before the first analysis of cardiac rhythm (with delivery of a defibrillator shock as appropriate). We found that there was no significant difference in the rate of survival with satisfactory functional status between the two EMS strategies of a brief period of CPR with early analysis of cardiac rhythm and a longer period of CPR with delayed analysis of rhythm. Subgroup and adjusted analyses also did not show any significant differences in the outcomes between the two study groups. We further explored the relationship between the rate of survival and the actual time to rhythm analysis and found that outcomes did not improve with increasing time to analysis. This finding suggests that there is no advantage of delaying the analysis of cardiac rhythm during EMS-administered CPR. Indeed, the data suggest that there may be a disadvantage of delaying the rhythm analysis in the subgroup of patients with a first rhythm of either ventricular tachycardia or ventricular fibrillation who have received CPR from a bystander. Overall, our data suggest that the administration of 2 minutes of CPR by EMS personnel before the first analysis of rhythm, which was suggested in the 2005 guidelines of the AHA–ILCOR, is unlikely to provide a greater benefit than CPR of shorter duration.
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The hypothesis that a brief period of initial CPR before analysis of cardiac rhythm could be beneficial is based primarily on the concept that a few minutes of chest compressions may increase myocardial perfusion, thus improving the metabolic state of the cardiac myocytes and enhancing the likelihood of successful defibrillation. Several studies in animals with experimentally induced ventricular fibrillation showed that the outcomes with delayed countershock after a period of chest compressions were better than the outcomes with earlier countershock, whereas other studies failed to show a benefit of CPR before shock. Five previous clinical studies also attempted to evaluate this issue, but all five had limitations involving the design or sample size, and none had findings that were definitive. Cobb et al., in a before-and-after study, showed that the rate of survival increased after the implementation of a policy that required 90 seconds of CPR before analysis of cardiac rhythm when an automated external defibrillator was used. Wik et al. conducted a randomized trial and found no significant difference between the outcomes after immediate defibrillation and those after 3 minutes of basic CPR before defibrillation, but the outcomes in a subgroup with response times exceeding 5 minutes were better after initial CPR than after immediate defibrillation. Randomized trials reported by Jacobs et al. and Baker et al. showed no significant difference in outcomes with early as compared with late defibrillation. Bradley et al. performed an observational analysis and found that CPR by EMS personnel for 46 to 195 seconds before defibrillation was weakly associated with an improved rate of survival.

The first site commenced the run-in phase in June 2007. All the sites stopped enrollment in November 2009, when the data and safety monitoring board recommended that the trial be stopped early because continuing recruitment was unlikely to change the outcome of the study. Of 13,460 patients screened, 10,365 were enrolled, and 10,153 underwent randomization. Of these, 195 were excluded from the data analysis when their cardiac arrest was confirmed to be due to drowning, strangulation, or electrocution, and 25 were excluded because the outcome with respect to the primary end point was unknown. Thus, 9933 patients were included in the primary data analysis.

Characteristics of the Two Study Groups

The early-analysis group comprised more patients than the later-analysis group (5290 vs. 4643) owing to early termination of the trial. The two study groups were evenly balanced with respect to baseline characteristics except that there were small group imbalances in the distribution of patients across sites; however, these would not have any appreciable effect on the results because of the cluster-crossover design, which yields treatment comparisons within clusters. Not all the scheduled cluster crossovers had occurred at the time of termination, although each cluster had crossed over at least once.

The median time to the analysis of cardiac rhythm was 42 seconds (interquartile range, 27 to 80) in the early-analysis group and 180 seconds (interquartile range, 151 to 190) in the later-analysis group. A majority of patients in each group received rhythm analysis within the targeted range for that group: 68% of patients in the early-analysis group received analysis of cardiac rhythm within the targeted range of 0 to 60 seconds and 60% of patients in the later-analysis group received analysis of cardiac rhythm within the targeted range of 150 to 210 seconds.

Primary and Secondary Outcomes

A total of 310 patients in the early-analysis group (5.9%) and 273 patients in the later-analysis group (5.9%) survived to hospital discharge with a modified Rankin score of 3 or less, with a cluster-adjusted difference between later cardiac analysis and early cardiac analysis of −0.2 percentage points. There was also no significant difference between the study groups with respect to any of the secondary outcomes. An analysis adjusted for potential confounders evaluated the effect of study group on survival and showed a difference of −0.3 percentage points (95% CI, −1.3 to 0.7) between later cardiac analysis and early cardiac analysis (P=0.61).

When the outcomes were analyzed on an as-treated basis, the rates of survival with satisfactory functional status were 6.0% among the 3982 patients in whom the analysis of cardiac rhythm was performed between 0 and 60 seconds and 5.9% among the 3115 patients in whom the analysis of cardiac rhythm was performed between 150 and 210 seconds (P=0.97). In an additional exploratory analysis, we evaluated the rate of survival as a function of the actual time to the first rhythm analysis, regardless of the study group. The chance of survival with satisfactory functional status did not improve with increasing time to the first analysis of cardiac rhythm, and among patients with an initial rhythm of ventricular tachycardia or ventricular fibrillation who received CPR from a bystander, the rate of survival tended to decline with increasing time to the first rhythm analysis.

Outcome Measures

The primary outcome was survival to hospital discharge with satisfactory functional status, defined as a score of 3 or less on the modified Rankin scale. This is a validated scale, ranging from 0 to 6, that is commonly used for measuring the performance of daily activities by people who have had a stroke. Lower scores represent better performance; scores of 4 or higher represent severe disability or death. Secondary outcomes were survival to discharge, survival to hospital admission, and return of spontaneous circulation at the time of arrival at the emergency department.

Statistical Analysis

We estimated that with enrollment of 13,239 patients who could be evaluated, the study would have 99.6% power to detect an improvement in the primary outcome from 5.4% with early analysis of heart rhythm to 7.4% with later analysis, assuming a group-sequential stopping rule at a two-sided alpha level of 0.05 with up to three interim analyses (O’Brien–Fleming boundaries). This calculation took into consideration the concurrent ITD portion of the trial, which required the enrollment of 14,154 patients who could be evaluated, in order to have 90% power to detect a 25% difference in the outcome between the two groups in that trial.

Analyses of the primary and secondary effectiveness outcomes were performed on the basis of a modified intention-to-treat principle with data from eligible patients in whom the cardiac arrest was not due to drowning, strangulation, or electrocution and for whom the primary outcome was known. An independent data and safety monitoring board reviewed the data at prespecified intervals and used a group-sequential stopping rule. The primary analysis compared the outcomes between the groups with the use of the Wald statistic for the treatment group in a generalized linear mixed model. The model included random effects for each of the clusters, accommodated the binary distribution of the outcome variable, and used a linear-link function to estimate an absolute difference in risk.

The between-group difference in the primary outcome, adjusted for baseline characteristics, was calculated with the use of a multiple linear regression model, with robust standard errors to accommodate clustering and the binary distribution of the outcome. Analyses of binary secondary outcomes and subgroup analyses were performed with the use of generalized-estimating-equation models to estimate differences in risk. Mean scores on the modified Rankin scale were compared between the two treatment groups with the use of a linear model.

We conducted further exploratory analyses of the data using kernel density estimators to estimate the distribution of time from the start of CPR to the actual analysis of cardiac rhythm, separately within treatment groups. The association between the primary outcome and the time of cardiac-rhythm analysis was explored with the use of smoothing splines, and confidence intervals were computed with the use of the bootstrap method.

The protocol was approved by the institutional review or research ethics boards at each participating site. The trial protocol, including the statistical analysis plan, is available at NEJM.org. All the authors vouch for the completeness and accuracy of the data and the analyses and for the fidelity of the study to the trial protocol.
Study Setting and Population

The trial was conducted at 150 of the 260 EMS agencies participating in the ROC. The trial agencies were selected because they had the capability to provide advanced cardiac life-support interventions and to record CPR process measures and because they met prespecified quality criteria during an initial run-in phase.

We included all persons 18 years of age or older who had an out-of-hospital cardiac arrest that was not the result of trauma and who were treated with defibrillation, delivery of chest compressions, or both by EMS providers. Persons were excluded if the arrest was witnessed by EMS personnel; if they had a blunt, penetrating, or burn-related injury; if the arrest was due to exsanguination; if they were pregnant; if they were prisoners; if they had an “opt-out” bracelet, indicating that they wished to opt out of the study; if they had “do not attempt resuscitation” orders; if the rhythm analysis was performed by police or a lay responder; or if they received initial treatment by an EMS agency that was not in the ROC. Patients were not required to provide informed consent; according to the regulations of the Food and Drug Administration and the Canadian Tri-Council agreement, this study qualified for exception from the requirements for informed consent because it involved research conducted during an emergency situation.
Randomization

Each of the 10 participating ROC centers (or sites) was divided into approximately 20 subunits, designated as “clusters,” according to EMS agency or geographic boundaries or according to defibrillator device, ambulance, station, or battalion. Randomization of clusters was stratified according to site. All episodes of cardiac arrest in a cluster were randomly assigned to one CPR strategy; after a set period of time, ranging from 3 to 12 months, all episodes in that cluster were then assigned to the other strategy. All the clusters were assigned to cross over to the other strategy one or more times during the study at fixed intervals; we estimated that approximately 100 patients would be included during each interval.
Study Intervention

Patients in the early-analysis group were assigned to receive 30 to 60 seconds of chest compressions and ventilations (sufficient time to place defibrillator electrodes) before electrocardiographic (ECG) analysis, and those in the late-analysis group were assigned to receive 3 minutes of chest compressions and ventilations before ECG analysis. The assigned intervention was implemented by the first qualified EMS provider to arrive at the scene (defibrillation-capable firefighter, emergency medical technician, or paramedic). The start and stop times for CPR were recorded by the responders, and the information was supplemented by the recording of defibrillator time.

The training of participating EMS providers emphasized uninterrupted chest compressions except for required ventilations, with compressions and ventilations applied in a 30:2 ratio, and specified that advanced airway devices were to be placed with minimal interruptions to compressions. Every 6 months, the EMS providers underwent some retraining that included written reminders, slide presentations, and Web-based modules. All ROC sites implemented high-quality electronic monitoring of the CPR process with the use of defibrillator hardware and software. Adherence to the protocol-specified performance targets and to the requirements for data submission was monitored throughout the study by a study monitoring committee, which provided regular feedback to sites.

Out-of-hospital cardiac arrest is a common and lethal problem, leading to an estimated 330,000 deaths each year in the United States and Canada. Overall, the rate of survival to hospital discharge among patients with an out-of-hospital cardiac arrest who are treated by emergency medical services (EMS) personnel is low but varies greatly, with rates ranging from 3.0% to 16.3%. This variation in the rate of survival can be attributed partly to local variations in the five key links in the chain of survival: rapid EMS access, early cardiopulmonary resuscitation (CPR), early defibrillation, early advanced cardiac life support, and effective care after resuscitation. Concerted efforts by EMS personnel to strengthen these links have led to only a slight increase in survival rates in recent years.
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The traditional approach to out-of-hospital cardiac arrest has been to emphasize early analysis of cardiac rhythm, with delivery of defibrillatory shocks, if indicated, as quickly as possible. It has been suggested, however, that many patients may benefit from a period of CPR before the first analysis of rhythm. The 2005 resuscitation guidelines from the American Heart Association–International Liaison Committee on Resuscitation (AHA–ILCOR) departed from its previous “shock first” strategy by suggesting that responders could provide 2 minutes of CPR before analysis of cardiac rhythm. These changes in the guidelines are supported by the findings of three clinical studies but are not supported by two others, and in the 2010 guidelines, the recommendation was modified to say that “there is inconsistent evidence to support or refute” such a delay in the analysis of cardiac rhythm. Therefore, the preferred initial approach remains uncertain. Our objective was to compare two approaches to the timing of CPR by EMS personnel — a brief period of manual chest compressions and ventilations with prompt initiation of rhythm analysis and defibrillation (early analysis) versus a longer period of compressions and ventilations before the first analysis of cardiac rhythm (later analysis).

Study Design and Oversight

A detailed description of the methods has been published previously. The Resuscitation Outcomes Consortium (ROC) is a clinical trial consortium comprising 10 U.S. and Canadian universities and their regional EMS systems. The ROC investigators designed the Prehospital Resuscitation Impedance Valve and Early Versus Delayed Analysis (ROC PRIMED) trial to study two randomized comparisons. The first comparison, in which early analysis of cardiac rhythm was compared with later rhythm analysis, is the subject of this article. The second, concurrent comparison, in which the use of an impedance threshold device (ITD) was compared with the use of a sham ITD, is reported elsewhere in this issue of the Journal. Most patients were enrolled simultaneously in both the early-analysis-versus-later-analysis component and the active-ITD-versus-sham-ITD component of the ROC PRIMED trial, although the two components had slightly different eligibility criteria.

Investigators were encouraged to practice evidence-based medicine and follow appropriate clinical practice guidelines in managing the care of their patients. The use, choices, and duration of antiplatelet therapy, as well as decisions about the use of other medical treatments and subsequent revascularization procedures, were left to the discretion of the treating physicians.

Study Outcomes
The primary efficacy outcome was the composite of cardiovascular death, myocardial infarction, or ischemic stroke.18 The primary safety outcome was major bleeding, according to the Thrombolysis in Myocardial Infarction (TIMI) definition. Prespecified secondary outcomes included the composite of cardiovascular death, myocardial infarction, ischemic stroke, or unstable angina; the composite of cardiovascular death, myocardial infarction, ischemic or hemorrhagic stroke, or fatal bleeding; and the composite of death from any cause, myocardial infarction, or ischemic or hemorrhagic stroke. Additional efficacy outcomes included the individual components of the primary efficacy outcome, unstable angina, and stent thrombosis. Additional safety outcomes included TIMI major or minor bleeding, major or clinically relevant nonmajor bleeding according to the International Society on Thrombosis and Haemostasis (ISTH) definitions, and severe or moderate bleeding according to the Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) definitions. Data on adverse events other than bleeding were also collected. The primary and secondary efficacy outcomes and the main safety outcome were adjudicated with the use of prespecified criteria by an independent clinical events committee whose members were unaware of the group assignments.

Statistical Analysis
Assuming a recruitment period of approximately 2 years, an average follow-up period of 1.25 years, and a rate of the primary efficacy outcome of 8% per year, we estimated that we would need to enroll 10,800 patients to achieve the desired target of 938 patients with a primary efficacy outcome. With this number of patients with events, we estimated that the study would have 80% power to detect a 20% reduction in relative risk with apixaban as compared with placebo at a one-sided alpha level of 0.005 and 93% power to detect the same reduction in risk at a one-sided alpha level of 0.025. In November 2010, after approximately 7000 patients had been recruited, the independent data monitoring committee recommended that the trial be stopped, owing to an excess of clinically important bleeding events with apixaban in the absence of a counterbalancing reduction in ischemic events. Recruitment was stopped on November 18, 2010. All the patients enrolled in the study were contacted and told to discontinue the study drug and schedule a final follow-up assessment. The trial database was locked on March 23, 2011. The intended treatment period, starting on the day of randomization and ending at the efficacy cutoff date (November 18, 2010), is the basis for the efficacy analyses. The actual treatment period, starting on the date the first dose of study drug was administered and ending 2 days after the last dose of study drug was administered, is the basis for the analyses of safety. A post hoc analysis was performed to assess the primary efficacy outcome during the actual treatment period.

Study Design
The Apixaban for Prevention of Acute Ischemic Events 2 (APPRAISE-2) trial was a double-blind, placebo-controlled, randomized clinical trial conducted at 858 sites in 39 countries. The study was approved by the institutional review board at each participating site. All participating patients gave written informed consent. The trial was supervised by a steering committee that included representatives from the sponsors (Bristol-Myers Squibb and Pfizer). The data were managed and all analyses were performed at the Duke Clinical Research Institute, Durham, North Carolina. All the authors designed the study, reviewed the data, participated in the analyses, and assume responsibility for the completeness and accuracy of the data and analyses and for the fidelity of the study to the protocol. The first author wrote the first draft of the manuscript, and all the authors provided comments on subsequent drafts and made the decision to submit the manuscript for publication.
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Study Population
The main inclusion criterion for the trial was an acute coronary syndrome (myocardial infarction, with or without ST-segment elevation, or unstable angina) within the previous 7 days, with symptoms of myocardial ischemia lasting 10 minutes or more with the patient at rest plus either elevated levels of cardiac biomarkers or dynamic ST-segment depression or elevation of 0.1 mV or more. Patients who met this criterion were eligible for the study if their condition was clinically stable and they were receiving standard treatment after the acute coronary syndrome, including aspirin or aspirin plus any P2Y12-receptor antagonist. Eligible patients were also required to have two or more of the following high-risk characteristics: an age of at least 65 years, diabetes mellitus, myocardial infarction within the previous 5 years, cerebrovascular disease, peripheral vascular disease, clinical heart failure or a left ventricular ejection fraction of less than 40% in association with the index event, impaired renal function with a calculated creatinine clearance of less than 60 ml per minute, and no revascularization after the index event.

Randomization and Study Regimen
Patients were randomly assigned, in a 1:1 ratio, to receive apixaban, at a dose of 5 mg twice daily, or matching placebo. Patients with an estimated creatinine clearance of less than 40 ml per minute at the time of randomization were randomly assigned to receive apixaban at a dose of 2.5 mg twice daily or matching placebo. Randomization was performed in a blinded fashion with the use of an interactive voice-response system, in permuted blocks of two, stratified according to site and according to planned long-term use of aspirin or aspirin plus a P2Y12-receptor antagonist. Patients who interrupted the study regimen during the course of the trial were encouraged to resume taking the assigned drug if and when possible.

Background
Apixaban, an oral, direct factor Xa inhibitor, may reduce the risk of recurrent ischemic events when added to antiplatelet therapy after an acute coronary syndrome.

Methods
We conducted a randomized, double-blind, placebo-controlled clinical trial comparing apixaban, at a dose of 5 mg twice daily, with placebo, in addition to standard antiplatelet therapy, in patients with a recent acute coronary syndrome and at least two additional risk factors for recurrent ischemic events.

Results
The trial was terminated prematurely after recruitment of 7392 patients because of an increase in major bleeding events with apixaban in the absence of a counterbalancing reduction in recurrent ischemic events. With a median follow-up of 241 days, the primary end point of cardiovascular death, myocardial infarction, or ischemic stroke occurred in 279 of the 3705 patients (7.5%) assigned to apixaban (13.2 events per 100 patient-years) and in 293 of the 3687 patients (7.9%) assigned to placebo (14.0 events per 100 patient-years) (hazard ratio with apixaban, 0.95; 95% confidence interval [CI], 0.80 to 1.11; P = 0.51). The primary safety outcome of major bleeding according to the Thrombolysis in Myocardial Infarction (TIMI) definition occurred in 46 of the 3673 patients (1.3%) who received at least one dose of apixaban (2.4 events per 100 patient-years) and in 18 of the 3642 patients (0.5%) who received at least one dose of placebo (0.9 events per 100 patient-years) (hazard ratio with apixaban, 2.59; 95% CI, 1.50 to 4.46; P = 0.001). A greater number of intracranial and fatal bleeding events occurred with apixaban than with placebo.

Conclusions
The addition of apixaban, at a dose of 5 mg twice daily, to antiplatelet therapy in highrisk patients after an acute coronary syndrome increased the number of major bleeding events without a significant reduction in recurrent ischemic events.

Patients with acute coronary syndromes frequently have recurrent ischemic events despite the use of currently recommended antiplatelet therapy, revascularization procedures as appropriate, and other evidence-based secondary preventive measures. Oral anticoagulation therapy with vitamin K antagonists reduces the incidence of recurrent ischemic events after myocardial infarction but also increases the risk of bleeding when it is added to aspirin or aspirin and clopidogrel. Apixaban, an orally active, selective, direct factor Xa inhibitor, has been shown to reduce the incidence of venous thromboembolism in patients undergoing orthopedic surgery and to prevent thromboembolic events in patients with atrial fibrillation who are not candidates for oral vitamin K antagonist therapy. We previously studied the use of apixaban, at doses of 5 to 20 mg daily, in patients who had had recent acute coronary syndromes and who were receiving aspirin or aspirin plus clopidogrel. Treatment with apixaban resulted in dose-related increases in bleeding events and a trend toward fewer ischemic events.

Considering both ischemic events and bleeding events, the preferred dose was thought to be 10 mg daily. Similar findings were observed with another factor Xa inhibitor, rivaroxaban, in a similar population. We therefore conducted a phase 3 trial to determine whether, in high-risk patients with an acute coronary syndrome, the benefit of apixaban in reducing ischemic events would outweigh the increased risk of bleeding.

Design
Prospective cohort study

Participants
31,823 women aged 48 to 83 years who were participants in the Swedish Mammography Cohort

Study “Medication”
Chocolate. Frequency of chocolate consumption was contrasted with incidence of heart failure. The women were followed from January 1, 1998, through December 31, 2006, for heart failure (HF) hospitalization or death. During this period, 419 women were hospitalized for incident HF (n=379) or died of HF (n=40).

Key Findings
Women consuming 1 to 3 servings of chocolate per month compared with no regular chocolate intake, had a 26% lower risk of heart failure. Those consuming 1 to 2 servings per week had a 32% decrease in risk. At higher levels of consumption, risk may increase, but the numbers did not reach statistical significance.

Practice Implications
Moderate consumption of chocolate (1–2 servings/week) might lower risk of heart failure in women, a finding that few will complain about.

Moderate consumption of chocolate (1 to 2 servings/week) might lower risk of heart failure in women, a finding that few will complain about.

A number of recent clinical trials utilizing high-polyphenol chocolate suggest that chocolate exerts a blood pressure–lowering effect in hypertensive individuals. A meta-analysis published in June 2010 combined data from 13 studies and concluded that “dark chocolate is superior to placebo in reducing systolic hypertension or diastolic prehypertension.”
What is striking about the Mostofsky study is that no “special” chocolate was required. Plain chocolate, or at least the chocolate commonly consumed in Sweden, was adequate to produce significant benefit. This is not to say that the special high-polyphenol chocolates may not produce even greater benefit.

While on this topic, mention must be made of the 2009 study by Janszky et al. In this earlier paper, 1,169 Swedish patients were followed after they had been hospitalized with a first heart attack. Chocolate consumption along with hospitalizations and mortality were tracked. Chocolate consumption had a strong inverse association with cardiac mortality. When compared with those of people who never eat chocolate, the hazard ratios were 0.73 for those consuming chocolate less than once per month, 0.56 up to once per week, and 0.34 for twice or more per week. In contrast, intake of other sweets was not associated with cardiac or total mortality.

Thus the data now clearly support our telling patients that weekly consumption of chocolate is not only acceptable but actually recommended for those at elevated risk for heart failure or myocardial infarction.

Doctors are often more interested in the health of a heart since it is very vital and important organ for living. Like the other parts or organ of the body, a heart may also have some disorder or ailment that will cause it from functioning well. The truth is that few tasks could be performed by a person with a heart failure or disorder. Nowadays, new innovations and improve treatment has been impose to let cardiac patients live nearly their normal lives. Also, more recently, several fresh equipment and process of operation had saved the lives of more people who were hopeless formerly. Here are some of the disorders or diseases associated with the heart.

Rheumatic Fever – it is a disease that could appear after an infection of the spherical bacteria. These kinds of bacteria are also the cause of tonsillitis and sore throat. This fever can create scars in tissues of the heart and eventually worst is cause a leak. This sort of ailment may be intense enough to allow the valve to function properly. Many times, the remedy of this injury is through operations. However, the one that is so damaged could be replacing by an artificial valve.

Heart Attack – as a person gets older, the arteries may be become firm or intolerant. This may be severe if it happens on the coronary arteries, for supply of blood from the heart could be blocked. This will result into chest pain and muscle hardening. Mostly person with heart attacks had recovered. They just have to rest for weeks or more to regain their energy and back into its normal life.

High Blood Pressure – heart is beating to supply the pressure needed to move the blood along the vessels. As mentioned earlier, when a person gets older, its arteries will be narrowed. This will allow the heart to push harder to let the blood flow and eventually, will cause high blood pressure. Drugs are being used by the doctors to relax one’s arterioles thus, lowering blood pressure.

Blue Babies – this disorder is present since birth and commonly noticed while you are still in infant. The reason for this is that there is a hole in the septum that divided the left and the right parts of the heart. The blue in color of the skin of a blue baby is due to the deoxygenated blood which is pump directly and flow from the right side and then to the left side of the heart. This bluish blood mixes with the oxygenated blood and then pumped all over the body. Operation can be done to close holes in the septum and remove the blue color.

Future medical and surgery skills could help prolong lives of the people. Series of studies and inventions had improved the facilities to sustain remedy and treatment for several heart disorders. Medical doctors have wished to discover an ideal and healthy artificial heart to replace with the damaged one. However, more recently, in 1967, a first heart transplant was performed. This was followed by another operation until such time that successful heart transplant operations have been increasing.