The 2011 Update Provides Critical Data Regarding Cardiovascular Quality of Care, Procedure Utilization, and Costs

The 2011 Update Provides Critical Data Regarding Cardiovascular Quality of Care, Procedure Utilization,and Costs

In light of the current national focus on healthcare utilization, costs, and quality, it is critical to monitor and understand the magnitude of healthcare delivery and costs, as well as the quality of healthcare delivery, related to CVDs. The Update provides these critical data in several sections.

Quality-of-Care Metrics for CVDs
In particular, quality data are available from the AHA’s “Get With The Guidelines” programs for coronary artery disease and heart failure and the American Stroke Association/ AHA’s “Get With the Guidelines” program for acute stroke. Similar data from the Veterans Healthcare Administration, national Medicare and Medicaid data and National Cardiovascular Data Registry Acute Coronary Treatment and Intervention Outcomes Network - “Get With The Guidelines”

Registry data are also reviewed. These data show impressive adherence with guideline recommendations for many, but not all, metrics of quality of care for these hospitalized patients. Data are also reviewed on screening for cardiovascular risk factor levels and control.

Cardiovascular Procedure Utilization and Costs
Chapter 21 provides data on trends and current usage of cardiovascular surgical and invasive procedures. For example, the total number of inpatient cardiovascular operations and procedures increased 27%, from 5 382 000 in 1997 to 6 846 000 in 2007 (National Heart, Lung, and Blood Institute computation based on National Center for Health Statistics annual data). Chapter 22 reviews current estimates of direct and indirect
healthcare costs related to CVDs, stroke, and related conditions using Medical Expenditure Panel Survey data. The total direct and indirect cost of CVD and stroke in the United States for 2007 is estimated to be $286 billion. This figure includes health expenditures (direct costs, which include the cost of physicians and other professionals, hospital services, prescribed medications, home health care, and other medical durables) and lost productivity resulting from mortality (indirect costs). By comparison, in 2008, the estimated cost of all cancer and benign neoplasms was $228 billion ($93 billion in direct costs, $19 billion in morbidity indirect costs, and $116 billion in mortality indirect costs). CVD costs more than any other diagnostic group.

The AHA, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current data available in the Statistics Update. The 2007 mortality data have been released. More information can be found at the National Center for Health Statistics Web site, http://www.cdc.gov/nchs/ data/nvsr/nvsr58/nvsr58_01.pdf. Finally, it must be noted that this annual Statistical Update is the product of an entire year’s worth of effort by dedicated professionals, volunteer physicians and scientists, and outstanding AHA staff members, without whom publication of this valuable resource would be impossible. Their contributions are gratefully acknowledged. Ve´ronique L. Roger, MD, MPH, FAHA Melanie B. Turner, MPH On behalf of the American Heart Association Heart Disease and Stroke Statistics Writing Group

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The 2011 Update Expands Data Coverage of the Obesity Epidemic and Its Antecedents and Consequences

● The estimated prevalence of overweight and obesity in US adults (20 years of age) is 149 300 000, which represents 67.3% of this group in 2008. Fully 33.7% of US adults are obese (body mass index 30 kg/m2). Men and women of all race/ethnic groups in the population are affected by the epidemic of overweight and obesity .

● Among children 2 to 19 years of age, 31.9% are overweight and obese (which represents 23 500 000 children), and 16.3% are obese (12 000 000 children). Mexican American boys and girls and African American girls are disproportionately affected. Over the past 3 decades, the prevalence of obesity in children 6 to 11 years of age has increased from 4% to more than 20%.

● Obesity (body mass index 30 kg/m2) is associated with marked excess mortality in the US population. Even more notable is the excess morbidity associated with overweight and obesity in terms of risk factor development and incidence of diabetes mellitus, CVD end points (including coronary heart disease, stroke, and heart failure), and numerous other health conditions, including asthma, cancer, degenerative joint disease, and many others.

● The prevalence of diabetes mellitus is increasing dramatically over time, in parallel with the increases in prevalence of overweight and obesity.

● On the basis of NHANES 2003–2006 data, the ageadjusted prevalence of metabolic syndrome, a cluster of major cardiovascular risk factors related to overweight/ obesity and insulin resistance, is 34% (35.1% among men and 32.6% among women).

● The proportion of youth (18 years of age) who report engaging in no regular physical activity is high, and the proportion increases with age. In 2007, among adolescents in grades 9 through 12, 29.9% of girls and 17.0% of boys reported that they had not engaged in 60 minutes of moderate-to-vigorous physical activity, defined as any activity that increased heart rate or breathing rate, even once in the previous 7 days, despite recommendations that children engage in such activity 5 days per week.

● Thirty-six percent of adults reported engaging in no vigorous activity (activity that causes heavy sweating and a large increase in breathing or heart rate).

● Data from NHANES indicate that between 1971 and 2004, average total energy consumption among US adults increased by 22% in women (from 1542 to 1886 kcal/d) and by 10% in men (from 2450 to 2693 kcal/d; ).

● The increases in calories consumed during this time period are attributable primarily to greater average carbohydrate intake, in particular, of starches, refined grains, and sugars. Other specific changes related to increased caloric intake in the United States include larger portion sizes, greater food quantity and calories per meal, and increased consumption of sugar-sweetened beverages, snacks, commercially prepared (especially fast food) meals, and higher energy-density foods.

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Prevalence and Control of Traditional Risk Factors Remains an Issue for Many Americans

● Data from the National Health and Nutrition Examination Survey (NHANES) 2005–2008 indicate that 33.5% of US adults 20 years of age have hypertension. This amounts to an estimated 76 400 000 US adults with hypertension. The prevalence of hypertension is nearly equal between men and women. African American adults have among the highest rates of hypertension in the world, at 44%. Among hypertensive adults, 80% are aware of their condition, 71% are using antihypertensive medication, and only 48% of those aware that they have hypertension have their condition controlled.

● Despite 4 decades of progress, in 2008, among Americans 18 years of age, 23.1% of men and 18.3% of women continued to be cigarette smokers. In 2009, 19.5% of students in grades 9 through 12 reported current tobacco use. The percentage of the nonsmoking population with detectable serum cotinine (indicating exposure to secondhand smoke) was 46.4% in 1999 to 2004, with declines occurring, and was highest for those 4 to 11 years of age (60.5%) and those 12 to 19 years of age (55.4%).

● An estimated 33 600 000 adults 20 years of age have total serum cholesterol levels 240 mg/dL, with a prevalence of 15.0% .

● In 2008, an estimated 18 300 000 Americans had diagnosed diabetes mellitus, representing 8.0% of the adult population. An additional 7 100 000 had undiagnosed diabetes mellitus, and 36.8% had prediabetes, with abnormal fasting glucose levels. African Americans, Mexican Americans, Hispanic/Latino individuals, and other ethnic minorities bear a strikingly disproportionate burden of diabetes mellitus in the United States .

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Death Rates From CVD Have Declined, Yet the Burden of Disease Remains High

● The 2007 overall death rate from CVD (International Classification of Diseases 10, I00 –I99) was 251.2 per 100 000. The rates were 294.0 per 100 000 for white males, 405.9 per 100 000 for black males, 205.7 per 100 000 for white females, and 286.1 per 100 000 for black females. From 1997 to 2007, the death rate from CVD declined 27.8%. Mortality data for 2007 show that CVD (I00 –I99; Q20–Q28) accounted for 33.6% (813 804) of all 2 243 712 deaths in 2007, or 1 of every 2.9 deaths in the United States.

● On the basis of 2007 mortality rate data, more than 2200 Americans die of CVD each day, an average of 1 death every 39 seconds. More than 150 000 Americans killed by CVD (I00 –I99) in 2007 were 65 years of age. In 2007, nearly 33% of deaths due to CVD occurred before the age of 75 years, which is well before the average life expectancy of 77.9 years.

● Coronary heart disease caused 1 of every 6 deaths in the United States in 2007. Coronary heart disease mortality in 2007 was 406 351. Each year, an estimated 785 000 Americans will have a new coronary attack, and 470 000 will have a recurrent attack. It is estimated that an additional 195 000 silent first myocardial infarctions occur each year. Approximately every 25 seconds, an American will have a coronary event, and approximately every minute, someone will die of one.

● Each year, 795 000 people experience a new or recurrent stroke. Approximately 610 000 of these are first attacks, and 185 000 are recurrent attacks. Mortality data from 2007 indicate that stroke accounted for 1 of every 18 deaths in the United States. On average, every 40 seconds, someone in the United States has a stroke. From 1997 to 2007, the stroke death rate fell 44.8%, and the actual number of stroke deaths declined 14.7%.

● In 2007, 1 in 9 death certificates (277 193 deaths) in the United States mentioned heart failure.

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American Heart Associations : Heart Disease and Stroke Statistical Update

Each year, the American Heart Association (AHA), in conjunction with the Centers or Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together the most up-to-date statistics on heart disease, stroke, other vascular diseases, and their risk factors and presents them in its Heart Disease and Stroke Statistical Update. The Statistical Update is a valuable resource for researchers, clinicians, healthcare policy makers, media professionals, the lay public, and many others who seek the best national data available on disease morbidity and mortality and the risks, quality of care, medical procedures and operations, and costs associated with the management of these diseases in a single document. Indeed, since 1999, the Statistical Update has been cited more than 8700 times in the literature (including citations of all annual versions). In 2009 alone, the various Statistical Updates were cited 1600 times (data from ISI Web of Science). In recent years, the Statistical Update has undergone some major changes with the addition of new chapters and major updates across multiple areas. For this year’s edition, the Statistics Committee, which produces the document for the AHA, updated all of the current chapters with the most recent nationally representative data and inclusion of relevant articles from the literature over the past year and added a new chapter detailing how family history and genetics play a role in cardiovascular disease (CVD) risk. Also, the 2011 Statistical Update is a major source for monitoring both cardiovascular health and disease in the population, with a focus on progress toward achievement of the AHA’s 2020 Impact Goals. Below are a few highlights from this year’s Update.

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Clinical Consequences of Myocardial Infarction

Clinical Consequences of Myocardial Infarction

A) Short Term

i. Cardiac Arrest; accounts for most acute deaths complicating myocardial infarction and is due to ventricular fibrillation. Treatment is immediate defibrillation. Understanding that, this one of the most lethal complications of acute MI led to the introduction of ICU monitoring for acute MI patients. This risk is usually seen during the first 24 hours of an MI. While VF arrest within the first 48 hours of an MI does not portend an adverse long-term prognosis, VF arrest beyond the first 48 hours does, and reflects extensive myocardial injury and poor underlying myocardial function. It also predicts a high future likelihood of recurrence of VF arrest.

ii. Congestive Heart Failure; A consequence of a sizeable myocardial infarction (> 25% cardiac muscle). The single most important determinant of prognosis after an acute STEMI. Carries a poor prognosis.

iii. Cardiogenic Shock; Seen when > 40% of myocardial muscle is injured. Marked by hypotension, poor peripheral perfusion and drop in urine output. Portends a very poor prognosis (50%-60% mortality) and is the cause of death in 60% of STEMI. Systolic BP < 80 mmHg, high filling pressure > 18 mmHg, and low cardiac index < 1.8L/min/M2). May also be the consequence of ruptured papillary muscle or interventricular septum.

iv. Rupture; Into the pericardial space resulting in immediate death due to pericardial tamponade. Usually complicating anterior or lateral wall MIs and in older individuals.

v. Pseudoaneurysm; A pseudoaneurysm is a confined free wall rupture held up by clot formation. Once identified it should be surgically corrected urgently. The difference between a pseudoaneurysm and a true aneurysm is that the wall of a true aneurysm contains myocardial tissue whereas the wall of a pseudoaneurysm is composed of clot and pericardial tissue.

vi. Ruptured Papillary Muscle; Resulting in acute mitral regurgitation. Seen more commonly after an inferior myocardialinfarction. Requiresurgent surgical repair.

vii. Ruptured Interventricular Septum; Usually after an acute anterior wall MI. Results in heart failure and requires urgent surgical therapy

viii. Aneurysm formation; This is an intermediate-term complication of a myocardial infarction. When a segment of myocardium becomes sluggish in its contraction secondary to a myocardial infarction it is described as hypokinetic. When the segment does not contract it is akinetic. When it bulges outward during systole; dyskinetic. This segment is aneurysmal and can lead to clot formation and ventricular arrhythmias.

B) Long Term
i. Heart failure; Coronary artery disease is the commonest cause of congestive heart failure in the Western economies

ii. Sudden cardiac death; Due to ventricular arrhythmias

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Clinical Consequences of Coronary Artery Disease

Coronary artery disease can present in a variety of ways. The classical presentation is with chest discomfort. Chest discomfort resulting from myocardial ischemia secondary to coronary artery disease is called angina pectoris (squeezing of the chest). Discomfort is diffuse and not localized and may radiate down the arms, as low as the umbilicus and up to the lower jaw. This may be associated with shortness of breath (dyspnea). This
discomfort is the result of myocardial ischemia however it is one of the last manifestations to appear. Due to the myocardium’s complete reliance on coronary blood flow for energy supply, within a few beats of coronary occlusion, diastolic and systolic dysfunction set in and the electrocardiogram begins to register abnormalities before the patient begins to experience angina pectoris. This explains why patients may describe
associated shortness of breath when they experience angina. The association of both symptoms together indicates that the myocardium fed by the narrowed vessel is sizable. The following are the more frequent clinical consequences of coronary artery disease. These “scenarios” may progress from one to another and their recognition allows for their proper management to preclude any potential lethal consequence. The term acute coronary syndrome refers to unstable angina, non ST-segment elevation and STsegment elevation myocardial infarction. One fourth of acute coronary syndrome patients are diagnosed with ST-segment elevation myocardial infarction, the remainders have unstable angina or non ST-segment MI (NSTEMI).

1. Stable Angina: Angina occurring predictably after exertion and relieved by rest. This is due to increased oxygen demand in the face of limited coronary flow. The more severe the narrowing, the less the amount of exertion required to induce ischemia and angina pectoris. As the narrowing becomes more severe, the amount of exertion required to precipitate angina becomes less. Certain types of exertion are classical in reproducing angina such as climbing stairs/slopes, walking in cold weather especially if accompanied by wind and after meals. The discomfort is pressure-like and diffuse, it peaks over minutes and when relieved by rest or sublingual nitroglycerine, it does so within 5-10 minutes. Some patients display individual variability in the amount of effort required to precipitate angina. This is called variable threshold angina where a component of
vasoconstriction may play a role in lowering the threshold for angina. Cardiac catheterization has shown that 25% of patients with stable angina have single vessel disease, 25% have two and 25% have three-vessel disease (defined as luminal narrowing of > 70%). Five to ten percent have left main disease and 15% have no
discernible obstruction. Treatment is by using beta-blockers to reduce myocardial O2 requirements, Ca++ channel blockers to vasodilate and reduce preload and afterload. Nitrates also vasodilate and reduce preload. When medical therapy fails, percutaneous intervention with balloon angioplasty or surgical revascularization may be required. Risk factor modification is equally important addressing dyslipidemia, hypertension, smoking, obesity and physical inactivity. The annual risk of death in this patient population is 1.7%-3% with a 1.4%-2.4% risk of a major ischemic event.

2. Unstable Angina: The diagnosis of unstable angina is a clinical one where patients with UA can present in one of three clinical scenarios; A) An acceleration from stable angina to one that occurs with less activity with more intensity and lasting longer. B) Angina at rest C) New onset angina usually with severe discomfort. Whereas the pathogenesis of ST-segment elevation myocardial infarction is total occlusion of the coronary vessel, the pathogenesis of UA is severe but not total occlusion of the culprit vessel. This is usually due to 1. plaque disruption with clot formation and interruption of distal blood flow, 2. Vasoconstriction, 3. mechanical occlusion, 4. inflammation, and 5. increased myocardial oxygen demand due to extracardiac causes (anemia, thyrotoxicosis) play variable roles in the pathogenesis of unstable angina. One year progression to death or myocardial infarction is between 7% and 14%. Patients older than 70 yrs., diabetic patients, and patients with vascular disease have a worse prognosis. Electrocardiographic determinants of prognosis include the magnitude of STsegment deviation as well as the presence of a left bundle branch block. Elevated serum troponin and C-reactive protein also portend a worse prognosis. The existence of these features should prompt a more aggressive approach. Since thrombus formation is an integral component in the pathogenesis of unstable angina, anticoagulants such as aspirin, heparin and more recently glycoprotein IIB/IIIA inhibitors are critical ingredients of the therapeutic armamentarium. Reduction of oxygen consumption using beta-blockers and nitrates are also used. A rise in one of the serum cardiac markers, troponin, portends a worse prognosis. Such patients are treated more aggressively with glycoprotein IIB/IIIA inhibitors and early cardiac catheterization.

3. Non-ST Elevated Myocardial Infarction. If patients present with chest discomfort and / or symptoms of a myocardial infarction (nausea, vomiting, diaphoresis, shortness of breath), have positive biomarkers for myocardial necrosis (CPK, CPK-MB and troponin, but without ST-segment elevation in the electrocardiogram, the diagnosis is non ST-elevated myocardial infarction (NSTEMI). Recent studies have shown that patients with NSTEMI constitute the majority (54%) of acute MIs patients admitted to the hospital. This study also showed that patients with NSTEMI had higher 1 year mortality (31%) than patients with ST-elevation MI (21%). Patients with NSTEMI tend to be older, have worse LV function, multi vessel disease and a history of acute coronary events. The pathophysiology of NSTEMI shares many of the features of UA i.e. clot on plaque, vasoconstriction, increased O2 demand, inflammation and progression of occlusive thrombus.

Management includes the use of heparin and glycoprotein IIB/IIIA inhibitors in addition to aspirin and beta-blockers. The importance of distinguishing ST-segment elevation from non ST-segment elevation myocardial infarction is that thrombolytic agents are not administered in NSTEMI and percutaneous intervention may be used acutely if the patient does not respond to medical therapy. 4. ST-Segment Elevation Myocardial Infarction. This is the other end of the spectrum of coronary syndromes. The etiology is complete occlusion of a coronary vessel from a clot developing on a recently ruptured plaque. These plaques are usually < 50% in diameter and are lipid rich. The ensuing activation of platelets and the coagulation cascade results in thrombus formation and occlusion of the vessel. Patients describe chest discomfort that is severe and often associated with nausea and vomiting. Discomfort typically lasts more than twenty minutes and does not respond to nitroglycerine. Radiation may occur down either arm, the lower jaw and to the back. Discomfort due to an acute MI does not radiate below the umbilicus or above the earlobes. Shortness of breath may indicate a large sized infarction. Up to 25% of patients, may not experience any discomfort when they suffer an infarction. The elderly and diabetic patients are more prone to having a silent myocardial infarction. Acute MIs, particularly in patients not receiving beta blockers of aspirin, tend to cluster between 6AM and 12PM. This circadian variation is thought to be due to circadian variation in levels of circulating corticosteroids and catecholamines. On examination, patients are uncomfortable and diaphoretic. They may exhibit pallor indicating decreased peripheral perfusion due to a drop in cardiac output and / or heightened sympathetic tone. Blood pressure may be normal, elevated due to discomfort and anxiety or reduced due to low cardiac output (especially if the right ventricle is involved) or the medications used to treat the patient’s condition. Jugular venous distension indicates right sided heart failure, the commonest cause being left-sided heart failure. Râles heard over the lung bases suggests left heart failure and is an ominous finding in patients suffering a myocardial infarction.

The WHO criteria for diagnosing an acute myocardial infarction is: Chest pain, serial elevation of cardiac enzymes and typical electrocardiographic features. The fulfillment of two out of three of these criteria establishes the diagnosis. A more recent definition for an acute, evolving or recent myocardial infarction requires the typical rise and fall of cardiac enzymes (troponin, CK-MB) along with one of the four following criteria;
1. Typical ischemic symptoms
2. ST-segment elevation or depression
3. Development of Q waves
4. Acute percutaneous intervention

Myocardial necrosis results in the release of non-specific and more specific enzymes. An estimation of the magnitude of myocardial necrosis can be determined by the degree of enzyme elevation. One of the first enzymes to climb is myoglobin. It peaks and falls back to baseline within one day of the MI, however myoglobin is very non-specific. The more cardio specific enzymes CK-MB and Troponins then begin to rise, CK-MB reaches a peak in 1-1 ½ day and is down to baseline in 4 days. Troponins peak in two days and fall
to baseline in 5-7 days. Hence, for the diagnosis of an MI that may have occurred 4-5 days ago, troponins are more helpful than CK-MB. Cardiac enzymes should display a characteristic rise followed by a fall back to baseline. The electrocardiogram displays characteristic changes. One of the first changes seen is elevation of the ST-segment and peaking of the T wave. The T wave then begins to invert and once irreversible myocardial necrosis sets in, Q waves begin to show. The STsegment then descends to baseline and the T wave may or may not normalize with time. Persistent ST-segment elevation may indicate formation of an aneurysm in the underlying myocardium. Patients with angina of non ST-segment elevation myocardial infarction (NSTEMI) display ST-segment depression and T wave changes but not the characteristic ST-segment elevation. Where myocardial infarction is involved, time is salvageable myocardium and every minute from the inception of symptoms counts. Irreversible injury begins to set in < one hour after occlusion of the offending vessel takes place. However myocardium can be salvaged as late as 12 hours after symptoms begin. This sets the stage for prompt intervention by one of two available methods of revascularization; thrombolytic (fibrinolytic) therapy and percutaneous intervention.

Tissue plasminogen activator is released by endothelial cells in response to clot formation. Plasminogen is cleaved to plasmin which in turn lyses fibrinogen breaking up formed or forming clot. This agent is given intravenously, however it cannot discriminate between a clot causing a myocardial infarction and a clot preventing a catastrophic hemorrhage, in for instance, the GI tract or the central nervous system. The risk / benefit ratio increases as time goes by. It is most effective when given the first four hours however it may be administered as late as twelve hours after symptoms began. Up to 80% of occluded coronary vessels are reperfused with fibrinolytic therapy leading to enhanced survival, improving prognosis and lowering complication rates. Recent studies have shown that acute percutaneous intervention with balloon tipped catheters (primary angioplasty) to revascularize occluded coronary vessels is equally as good as if not safer than thrombolytic therapy as long as its employment does not lengthen the critical time to intervention. Up to 30% of patients with myocardial infarction have a contraindication to receive fibrinolytic therapy and may benefit from primary angioplasty.

Adjunctive treatment includes aspirin, heparin, analgesics and beta blockers. Recently administration of afterload reducing agents angiotensin converting enzyme inhibitors (ACE-inhibitors) and cholesterol reducing hydroxymethylglutaryl coenzyme-A reductase inhibitors (statins) has been shown to portend favorably on patients with acute MI. Mortality from ST-elevated MI has declined over the last 40 years. This is in part due to the introduction of coronary care units, use of invasive monitoring when appropriate, thrombolytic therapy and direct acute revascularization. Large studies report in-hospital mortalities of 6.5%-7% whereas community based observation yield a15%-20% mortality.

5. Silent Ischemia. Impaired coronary flow may occur without symptoms. This syndrome can be seen in up to 40% of patients with classical angina pectoris and in up to 10% of patients with no symptoms of angina at all. Diabetic patients have a higher incidence of silent ischemia. Angina is a warning symptom without which serious underlying coronary disease is often overlooked. Hence patients with silent ischemia have a worse prognosis than those with angina pectoris.

6. Sudden Cardiac Death. Patients with coronary artery disease can present for the first time with a lethal arrhythmia; ventricular fibrillation. The definition of Sudden Cardiac Death is natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour of the onset of acute symptoms. Preexisting heart disease may or may not have been known to be present, but the time and mode of death are unexpected. Ischemia plays an important role in generating ventricular fibrillation, the lethal arrhythmia that leads to sudden cardiac death. It may occur immediately as a result of plaque rupture and occlusion of a critical vessel or after the onset of a myocardial infarction. Patients with a history of a myocardial infarction and myocardial damage are also predisposed to ventricular arrhythmias (primary ventricular fibrillation arrest).

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