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Cardiovascular Disease

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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-.

Cardiovascular Disease
Authors

Edgardo Olvera Lopez1; Arif Jan2.

Affiliations
1 NYC Health + Hospitals / Lincoln
2 Drexel University

Last Update: June 20, 2019.

Introduction
The cardiovascular system consists of the heart and blood vessels.[1] There is a wide array of problems that may arise
within the cardiovascular system, for example, endocarditis, rheumatic heart disease, abnormalities in the conduction
system, among others, cardiovascular disease (CVD) or heart disease refer to the following 4 entities that are the focus
of this article[2]:

1. Coronary artery disease (CAD): Sometimes referred to as Coronary Heart Disease (CHD), results
from decreased myocardial perfusion that causes angina, myocardial infarction (MI), and/or heart failure. It
accounts for one-third to one-half of the cases of CVD.

2. Cerebrovascular disease (CVD): Including stroke and transient ischemic attack (TIA)

3. Peripheral artery disease (PAD): Particularly arterial disease involving the limbs that may result in claudication

4. Aortic atherosclerosis: Including thoracic and abdominal aneurysms

Etiology
Although CVD may directly arise from different etiologies such as emboli in a patient with atrial fibrillation resulting
in ischemic stroke, rheumatic fever causing valvular heart disease, among others, addressing risks factors associated to
the development of atherosclerosis is most important because it is a common denominator in the pathophysiology of
CVD.

The industrialization of the economy with a resultant shift from physically demanding to sedentary jobs, along with the
current consumerism and technology-driven culture that is related to longer work hours, longer commutes, and less
leisure time for recreational activities, may explain the significant and steady increase in the rates of CVD during the
last few decades. Specifically, physical inactivity, intake of a high-calorie diet, saturated fats, and sugars are
associated with the development of atherosclerosis and other metabolic disturbances like metabolic syndrome, diabetes
mellitus, and hypertension that are highly prevalent in people with CVD.[3][2][4][5]

According to the INTERHEART study that included subjects from 52 countries, including high, middle, and low-
income countries, 9 modifiable risks factors accounted for 90% of the risk of having a first MI: smoking, dyslipidemia,
hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits and vegetables, regular alcohol
consumption, and physical inactivity. It is important to mention that in this study 36% of the population-attributable

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risk of MI was accounted to smoking.[6]

Other large cohort studies like the Framingham Heart Study[7] and the Third National Health and Nutrition
Examination Survey (NHANES III)[5] have also found a strong association and predictive value of dyslipidemia, high
blood pressure, smoking, and glucose intolerance. Sixty percent to 90% of CHD events occurred in subjects with at
least one risk factor.

These findings have been translated into health promotion programs by the American Heart Association with emphasis
on seven recommendations to decrease the risk of CVD: avoiding smoking, being physically active, eating healthy, and
keeping normal blood pressure, body weight, glucose, and cholesterol levels.[8][9]

On the other hand, non-modifiable factors as family history, age, and gender have different implications.[4][7] Family
history, particularly premature atherosclerotic disease defined as CVD or death from CVD in a first-degree relative
before 55 years (in males) or 65 years (in females) is considered an independent risk factor.[10] There is also
suggestive evidence that the presence of CVD risk factors may differently influence gender.[4][7] For instance,
diabetes and smoking more than 20 cigarettes per day had increased CVD risk in women compared to men.[11]
Prevalence of CVD increases significantly with each decade of life.[12]

The presence of HIV (human immunodeficiency virus),[13] history of mediastinal or chest wall radiation,
[14] microalbuminuria,[15], increased inflammatory markers[16][17] have also been associated with an increased rate
and incidence of CVD.

Pointing out specific diet factors like meat consumption, fiber, and coffee and their relation to CVD remains
controversial due to significant bias and residual confounding encountered in epidemiological studies.[18][19]

Epidemiology
Cardiovascular diseases (CVD) remain among the 2 leading causes of death in the United States since 1975 with
633,842 deaths or 1 in every 4 deaths, heart disease occupied the leading cause of death in 2015 followed by 595,930
deaths related to cancer.[2] CVD is also the number 1 cause of death globally with an estimated 17.7 million deaths in
2015, according to the World Health Organization (WHO). The burden of CVD further extends as it is considered the
most costly disease even ahead of Alzheimer disease and diabetes with calculated indirect costs of $237 billion dollars
per year and a projected increased to $368 billion by 2035.[20]

Although the age-adjusted rate and acute mortality from MI have been declining over time, reflecting the progress in
diagnosis and treatment during the last couple of decades, the risk of heart disease remains high with a calculated 50%
risk by age 45 in the general population.[7][21] The incidence significantly increases with age with some variations
between genders as the incidence is higher in men at younger ages.[2] The difference in incidence narrows
progressively in the post-menopausal state.[2]

Pathophysiology
Atherosclerosis is the pathogenic process in the arteries and the aorta that can potentially cause disease as a
consequence of decreased or absent blood flow from stenosis of the blood vessels.[22]

It involves multiple factors dyslipidemia, immunologic phenomena, inflammation, and endothelial dysfunction. These
factors are believed to trigger the formation of fatty streak, which is the hallmark in the development of the
atherosclerotic plaque[23]; a progressive process that may occur as early as in the childhood.[24] This process

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comprises intimal thickening with subsequent accumulation of lipid-laden macrophages (foam cells) and extracellular
matrix, followed by aggregation and proliferation of smooth muscle cells constituting the formation of the atheroma
plaque.[25] As this lesions continue to expand, apoptosis of the deep layers can occur, precipitating further macrophage
recruitment that can become calcified and transition to atherosclerotic plaques.[26]

Other mechanisms like arterial remodeling and intra-plaque hemorrhage play an important role in the delay and
accelerated the progression of atherosclerotic CVD but are beyond the purpose of this article.[27]

History and Physical

The clinical presentation of cardiovascular diseases can range from asymptomatic (e.g., silent ischemia, angiographic
evidence of coronary artery disease without symptoms, among others) to classic presentations as when patients present
with typical anginal chest pain consistent of myocardial infarction and/or those suffering from acute CVA presenting
with focal neurological deficits of sudden onset.[28][29][28]

Historically, coronary artery disease typically presents with angina that is a pain of substernal location, described as a
crushing or pressure in nature, that may radiate to the medial aspect of the left upper extremity, to the neck or the jaw
and that can be associated with nausea, vomiting, palpitations, diaphoresis, syncope or even sudden death.
[30] Physicians and other health care providers should be aware of possible variations in symptom presentation for
these patients and maintain a high index of suspicion despite an atypical presentation, for example, dizziness and
nausea as the only presenting symptoms in patients having an acute MI[31]), particularly in people with a
known history of CAD/MI and for those with the presence of CVD risk factors.[32][33][34][33][32] Additional chest
pain features suggestive of ischemic etiology are the exacerbation with exercise and or activity and resolution with rest
or nitroglycerin.[35]

Neurologic deficits are the hallmark of cerebrovascular disease including TIA and stroke where the key differentiating
factor is the resolution of symptoms within 24 hours for patients with TIA.[36] Although the specific symptoms
depend on the affected area of the brain, the sudden onset of extremity weakness, dysarthria, and facial droop are
among the most commonly reported symptoms that raise concern for a diagnosis of a stroke.[37][38] Ataxia,
nystagmus and other subtle symptoms as dizziness, headache, syncope, nausea or vomiting are among the most
reported symptoms with people with posterior circulation strokes challenging to correlate and that require highly
suspicion in patients with risks factors.[39]

Patients with PAD may present with claudication of the limbs, described as a cramp-like muscle pain precipitated by
increased blood flow demand during exercise that typically subsides with rest.[40] Severe PAD might present with
color changes of the skin and changes in temperature.[41]

Most patients with thoracic aortic aneurysm will be asymptomatic, but symptoms can develop as it progresses from
subtle symptoms from compression to surrounding tissues causing cough, shortness of breath or dysphonia, to the acute
presentation of sudden crushing chest or back pain due to acute rupture.[42] The same is true for abdominal aortic
aneurysms (AAA) that cause no symptoms in early stages to the acute presentation of sudden onset of abdominal pain
or syncope from acute rupture.[43]

A thorough physical examination is paramount for the diagnosis of CVD. Starting with a general inspection to look for
signs of distress as in patients with angina or with decompensated heart failure, or chronic skin changes from PAD.
Carotid examination with the patient on supine position and the back at 30 degrees for the palpation and auscultation of
carotid pulses, bruits and to evaluate for jugular venous pulsations on the neck is essential. Precordial examination

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starting with inspection, followed by palpation looking for chest wall tenderness, thrills, and identification of the point
of maximal impulse should then be performed before auscultating the precordium. Heart sounds auscultation starts in
the aortic area with the identification of the S1 and S2 sounds followed by characterization of murmurs if present.
Paying attention to changes with inspirations and maneuvers to correctly characterize heart murmurs is encouraged.
Palpating peripheral pulses with bilateral examination and comparison when applicable is an integral part of the CVD
examination.[44]

Evaluation
Thorough clinical history and physical exam directed but not limited to the cardiovascular system are the hallmarks for
the diagnosis of CVD. Specifically, a history compatible with obesity, angina, decreased exercise tolerance, orthopnea,
paroxysmal nocturnal dyspnea, syncope or presyncope, and claudication should prompt the clinician to obtain a more
detailed history and physical exam and, if pertinent, obtain ancillary diagnostic test according to the clinical scenario
(e.g., electrocardiogram and cardiac enzymes for patients presenting with chest pain).

Besides a diagnosis prompted by clinical suspicion, most of the efforts should be oriented for primary prevention by
targeting people with the presence of risk factors and treat modifiable risk factors by all available means. All patient
starting at age 20 should be engaged in the discussion of CVD risk factors and lipid measurement.[9] Several
calculators that use LDL-cholesterol and HDL-cholesterol levels and the presence of other risk factors calculate a 10-
year or 30-year CVD score to determine if additional therapies like the use of statins and aspirin are indicated for
primary prevention, generally indicated if such risk is more than ten percent.[10] Like other risk assessment tools, the
use of this calculators have some limitations, and it is recommended to exert precaution when assessing patients with
diabetes and familial hypercholesterolemia as their risk can be underestimated. Another limitation to their use is that
people older than 79 were usually excluded from the cohorts where these calculators were formulated, and
individualized approach for these populations is recommended by discussing risk and benefits of adjunctive therapies
and particular consideration of life expectancy. Some experts recommend a reassessment of CVD risk every 4 to 6
years.[9]

Preventative measures like following healthy food habits, avoiding overweight and following an active lifestyle are
pertinent in all patients, particularly for people with non-modifiable risk factors such as family history of premature
CHD or post-menopause.[9][8]

The use of inflammatory markers and other risk assessment methods as coronary artery calcification score (CAC) are
under research and have limited applications that their use should not replace the identification of people with known
risk factors, nonetheless these resources remain as promising tools in the future of primary prevention by detecting
people with subclinical atherosclerosis at risk for CVD.[45]

Treatment / Management
Management of CVD is very extensive depending on the clinical situation (catheter-directed thrombolysis for acute
ischemic stroke, angioplasty for peripheral vascular disease, coronary stenting for CHD); however, patients with
known CVD should be strongly educated on the need for secondary prevention by risk factor and lifestyle
modification.[9][46]

Prognosis
The prognosis and burden of CVD have been discussed in other sections.

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Complications
The most feared complication from CVD is death and, as explained above, despite multiple discoveries in the last
decades CVD remains in the top leading causes of death all over the world owing to the alarming prevalence of CVD
in the population.[2] Other complications as the need for longer hospitalizations, physical disability and increased costs
of care are significant and are the focus for health-care policymakers as it is believed they will continue to increase in
the coming decades.[20]

For people with heart failure with reduced ejection fraction (HFreEF) of less than 35%, as the risk of life-threatening
arrhythmias is exceedingly high in these patients, current guidelines recommend the implantation of an implantable-
cardioverter defibrillator (ICD) for those with symptoms equivalent to a New York Heart Association (NYHA) Class
II-IV despite maximal tolerated medical therapy.[47]

Strokes can leave people with severe disabling sequelae like dysarthria or aphasia, dysphagia, focal or generalized
muscle weakness or paresis that can be temporal or cause permanent physical disability that may lead to a complete
bedbound state due to hemiplegia with added complications secondary to immobility as is the higher risk of developing
urinary tract infections and/or risk for thromboembolic events.[48][49]

There is an increased risk of all-cause death for people with PAD compared to those without evidence of peripheral
disease.[50] Chronic wounds, physical limitation, and limb ischemia are among other complications from PAD.[51]

Consultations
An interprofessional approach that involves primary care doctors, nurses, dietitians, cardiologists, neurologists, and
other specialists is likely to improve outcomes. This has been shown to be beneficial in patients with heart failure,
[52] coronary disease,[53] and current investigations to assess the impact on other forms of CVD are under planning
and promise encouraging results.

Deterrence and Patient Education

Efforts should be directed toward primary prevention by leading a healthy lifestyle, and an appropriate diet starting as
early as possible with the goal of delay or avoid the initiation of atherosclerosis as it relates to the future risk of CVD.
The AHA developed the concept of "ideal cardiovascular health" defined by the presence of[8]:

Ideal health behaviors: Nonsmoking, body mass index less than 25 kg/m2, physical activity at goal levels,
and the pursuit of a diet consistent with current guideline recommendations

Ideal health factors: Untreated total cholesterol less than 200 mg/dL, untreated blood pressure less than 120/80
mm Hg, and fasting blood glucose less than 100 mg/dL) with the goal to improve the health of all Americans
with an expected decrease in deaths from CVD by 20%

Specific attention should be made to people at higher risk for CVD as are people with diabetes, hypertension,
hyperlipidemia, smokers, and obese patients. Risk factors modification by controlling their medical conditions,
avoiding smoking, taking appropriate measures to lose weight and maintaining an active lifestyle is of
extreme importance.[8][9][10] The recommendations on the use of statins and low-dose aspirin for primary and
secondary prevention has been discussed in other sections.

Pearls and Other Issues

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Cardiovascular disease generally refers to 4 general entities: CAD, CVD, PVD, and aortic atherosclerosis.

CVD is the main cause of death globally.

Measures aimed to prevent the progression of atherosclerosis are the hallmark for primary prevention of CVD.

Risk factor and lifestyle modification are paramount in the prevention of CVD.

Enhancing Healthcare Team Outcomes

An interprofessional and patient-oriented approach can help to improve outcomes for people with cardiovascular
disease as shown in patients with heart failure (HF) who had better outcomes when the interprofessional involvement
of nurses, dietitians, pharmacists, and other health professionals was used (Class 1A).[52]

Similarly, positive results were obtained in people in an intervention group who were followed by an interprofessional
team comprised of pharmacists, nurses and a team of different physicians. This group had a reduction in all-cause
mortality associated with CAD by 76% compared to the control group.[53] Healthcare workers should educate the
public on lifestyle changes and reduce the modifiable risk factors for heart disease to a minimum.

Questions
To access free multiple choice questions on this topic, click here.

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