Sunteți pe pagina 1din 47

ACUTE PERICARDITIS

MYOCARDIAL INFARCTION
UNSTABLE ANGINA
PRIMARY PREVENTION aimed at either delaying atheroma
formation or causing regression of established lesions in persons
who have never suffered a serious complication of
atherosclerotic coronary artery disease

SECONDARY PREVENTION intended to prevent recurrence of


events such as myocardial infarction in patients with
symptomatic disease

TERTIARY PREVENTION to avert or reduce complications


Control of risk factors is the cornerstone of
primary and secondary prevention
weight reduction
and increased
exercise
moderation of
control of
alcohol
hypertension
consumption

Recommendations for most importantly,


primary prevention of lowering total and
abstention from atherosclerosis-
LDL blood
or cessation of related complications
in adults, based on cholesterol levels
cigarette smoking
risk factor while increasing
modification: HDL
Cessation of rates of first myocardial
cigarette smoking infarction or death from
reduces the risk of coronary heart disease
a second coronary also decline within the
event within 612 first few years following
months cessation

the risk of a new


myocardial infarction or
After 15 years of death from coronary heart
cessation disease in former smokers
is similar to that for those
who have never smoked
Advice from a physician to quit smoking,
particularly around an acute illness, is a
powerful trigger for cessation attempts, with
up to half of patients who are advised to quit
making a cessation effort

Other triggers include the cost of cigarettes,


media campaigns, and changes in rules to restrict
smoking in the workplace
Ask
Systematically identify all tobacco users at every
visit
Advise
Strongly urge all smokers to quit
provided a clear, strong, and personalized physician
message that smoking is an important health
concern

Assess
Identify smokers willing to quit

Assist the patient in quitting


quit date should be negotiated, usually not the day
of the visit but within the next few weeks

Arrange follow-up contact


Note: BMI, body mass index; DASH, Dietary Approaches to Stop
Hypertension (trial).
Potassium supplementation
Vegetarian diet
Fiber intake
Decreased dietary fat intake
Fish oil and omega-3-polyunsaturated FA
Diet high in carbohydrate
Antioxidants
Caffeine
Inhibition of free radical formation
At least and low-density lipoprotein oxidation
seven Inhibition of proliferation of vascular
possible smooth muscle cells
Inhibition of platelet aggregation and
mechanisms arterial thrombosis
have been Reduction in renal vascular resistance
proposed by and increase in glomerular filtration
which rate
Vascular relaxation by enhanced
potassium vascular Na+/ K+adenosine
may lower BP triphosphatase activity
and protect A natriuresis
against CVDs: A reduction in pressor sensitivity to
sodium
Potassium and calcium
supplementation have
inconsistent, modest
antihypertensive effects, and,
independent of blood pressure,
potassium supplementation may
be associated with reduced stroke
mortality

Diets deficient in potassium,


calcium, and magnesium are
associated with higher blood
pressures and a higher
prevalence of hypertension
Vegetarians If hypertensives
tend to consumed a
vegetarian diet
have low under controlled
BP, but the conditions for 6
weeks, an average
reason for fall in systolic BP of
this is 5 mm Hg was
observed.
unknown
Fiber intake of less than 12 g
per day was associated with a
One feature of a 1.57 increased relative risk for
vegetarian diet is the developing hypertension over a
increased amount of 4-year follow-up as compared
to the risk associated with an
fiber intake of more than 24 g per
day

The benefits found


The benefits of
with increased fruits
increased dietary fiber
and vegetables in the
may reflect decreases
DASH diet could reflect
in body weight and
the increase in fiber
plasma insulin levels
from 9 to 31 g per day
Inkeeping with the potential contribution of the
low saturated fat content of the DASH diet, other
smaller studies have shown a lowering of BP with a
low-fat diet

The type of fat may also be important


As a component of the cardiovascular beneficial
Mediterranean diet, olive oil may lower BP because of
its high content of monounsaturated fatty acids or
antioxidant polyphenols
Higher intakes of the polyunsaturated linoleic acid may
also lower BP and reduce the incidence of hypertension
Similarly, both an antihypertensive effect and a protective effect against stroke have
been seen with docosahexaenoic acid, one of the major omega-3-poly-unsaturated
fatty acids (PUFA) in cold-water fish, albacore tuna, herring, mackerel, rainbow trout,
salmon, sardines

These effects may derive from improvements in endothelium-independent


vasodilator mechanisms and decreases in concentrations of soluble adhesion
molecules

Fortunately, just eating more fish reduces the risk for coronary disease,
stroke, and all-cause mortality
may improve insulin action
and glycemic control,
Diet high in particularly in patients with
carbohydrate (>50%) mild hyperglycemia

In patients with more reduced carbohydrate intake


severe fasting (<45% of total calories) and
hyperglycemia or with greater reliance on
triglyceride elevations monounsaturated fats may
aggravated by high- be preferable
carbohydrate diets
Vitamin C improves endothelial-dependent
vasodilation

Supplements of vitamin C (500 mg per day)


reduced systolic BP by 2.0 mm Hg in 40 older
adults (Fotherby et al., 2000) and by 1.3 mm Hg
in 45 middle-aged hypertensives

Vitamin E supplements do not appear to


lower BP in treated hypertensives
Caffeine, consumed daily by approximately
80% of adults in coffee, tea, or cola drinks,
acutely raises both systolic and diastolic BP
from 5 to 15 mm Hg for several hours in
some but not all subjects, more in
hypertensives than normotensives

Teamay raise BP even more than would be


expected from its caffeine content

***The effect likely reflects vasoconstriction by antagonism of


endogenous adenosine and increased arterial wave reflection
decreases mild decrease in
myocardial blood pressure
contractility and and a
ETHANOL
causes compensatory
peripheral increase in
vasodilation, cardiac output

Drinking of 60 g of ethanol, the amount contained in five


usual portions of beer (12 oz), wine (4 oz), or whiskey
(1.5 oz), induces an immediate fall in BP averaging 4/4
mm Hg f

Although the apparent pressor effect may be exaggerated


by a considerable white-coat effect the BP does rise
during heavy binge drinking
Carefully assess alcohol intake, as some people
drink well beyond moderate amounts without
being aware of their excessive consumption or its
deleterious effects

If intake is more than one portion per day in


women or two per day in men, advise a reduction
to that level. Women should be advised of an
increase in the prevalence of breast cancer with
more than one portion (10 g alcohol) per day

For most people who consume moderate amounts


of alcohol on a regular, daily basis, no change is
needed
Alcohol use in persons
consuming three or more
drinks per day (a standard
drink contains ~14 g
ethanol) is associated
with higher blood
pressures

reduction of alcohol
consumption is associated
with a reduction of blood
pressure

Mechanisms by which alcohol may affect blood pressure


have not been established
Exercise

reduction in plasma
triglycerides and has beneficial
reduction in blood
low-density effects on glucose
pressure, both in improvement in
lipoprotein metabolism and the
association with or atherogenic lipid
cholesterol and sensitivity of
independently of profiles
elevation of high- skeletal muscle to
weight loss
density lipoprotein insulin
cholesterol

It is not necessary for the obese patient to increase maximal oxygen uptake
by strenuous exercise to derive benefit from exercise: metabolic evidence of
improvement in fitness is achieved with less vigorous exercise such as walking
increased distances and swimming
Exercise
lowers BP through multiple
mechanisms, including the following:
Lower sympathetic nerve traffic accompanied
by potentiation of the baroreceptor reflex
Reduced arterial stiffness and increased total
systemic arterial compliance
Increased release of endothelium-derived
nitric oxide that may be related to lower
plasma cholesterol
Increased insulin sensitivity
LDL Cholesterol Goals and Cutpoints for Therapeutic Lifestyle
Changes (TLC) in Different Risk Categories
The first maneuver to achieve
the LDL goal involves
therapeutic lifestyle changes
(TLC), including specific diet
and exercise recommendations
established by the guidelines

In patients with triglycerides >


2.6 mmol/L (>200 mg/dL), ATP
According to ATP III criteria, III guidelines specify a
those with LDL levels exceeding secondary goal for therapy,
goal for their risk group by >0.8 "non-HDL cholesterol" (simply,
mmol/L (>30 mg/dL) merit the HDL cholesterol level
consideration for drug therapy subtracted from the total
cholesterol)
accelerates coronary and peripheral
atherosclerosis

frequently associated with dyslipidemias and


increases in the risk of angina, MI, and sudden
coronary death

Aggressive control of the dyslipidemia (target


LDL cholesterol <70 mg/dL) and hypertension
(target BP 120/80 or less) that are frequently
found in diabetic patients is essential
Treatment of hyperlipidemia:
(1) lower the LDL cholesterol,
(2) raise the HDL cholesterol, and
(3) decrease the triglycerides

*The rationale for these goals is that the risk of CHD is similar
to that in patients without diabetes who have had a prior MI.
Advances in secondary prevention
have resulted in increasingly
effective measures to reduce
recurrent MI and cardiovascular
death
Secondary prevention should be
conscientiously applied after acute
MI
A fasting lipid profile is
recommended on admission, and
lipid-lowering therapy, typically with
a statin, is begun in the hospital,
generally with an LDL cholesterol
goal of less than 70 mg/dL .
Continued smoking doubles the subsequent
mortality risk after acute MI, and smoking
cessation reduces the risk of reinfarction and
death within 1 year.
An individualized smoking cessation plan
should be formulated, including pharmacologic
aids (nicotine gum and patches, bupropion)
Antiplatelet therapy should consist of
aspirin, given on a long-term basis to all
patients without contraindications
(maintenance dose, 75 to 162 mg/day).

Clopidogrel (75 mg/day) is given to patients who received PCI


with stenting and is also appropriate for others at higher risk
for recurrent vascular events.
Therapy is recommended for a minimum of 1 month after a
bare metal stent, for at least 3 months for sirolimus-eluting
stents, and for at least 6 months for paclitaxel-eluting stents.
If patients are not at high risk of bleeding, therapy is
continued for up to 1 year or more.
Anticoagulant therapy (i.e., warfarin, with an
international normalized ratio goal of 2.0 to 3.0)
indicated after acute MI for patients unable to take
antiplatelet therapy (aspirin or clopidogrel), for those
with persistent or paroxysmal AF, for those with LV
thrombus, and for those who have suffered a systemic
or pulmonary embolism.
Anticoagulants also may be considered for patients
with extensive wall motion abnormalities and
markedly depressed ejection fraction with or
without heart failure
Data on the benefit of warfarin instead of or in
addition to aspirin are inconclusive
Long-term -blocker therapy is
strongly recommended for all MI
survivors without uncompensated
heart failure or other
contraindications.
Long-term therapy in patients at
low risk (normal ventricular
function, successful recanalization,
absence of arrhythmias) is
reasonable but not mandatory.
Nitroglycerin (0.4 mg) is prescribed
routinely for sublingual or buccal
administration for acute anginal attacks.
Longer-acting oral therapy (isosorbide
mononitrate, 30 to 60 mg orally every
morning, or dinitrate, 10 to 40 mg orally
two to three times daily) or topical
nitroglycerin (e.g., start 0.5 inch, can
titrate up to 2 inches, every 6 hours for 2
days) may be added to treatment regimens
for angina or heart failure in selected
patients.
Calcium-channel blockers are negatively
inotropic and are not routinely given on a long-
term basis; however, they may be given to
selected patients without LV dysfunction
(ejection fraction >0.40) who are intolerant of
-blockers and who require these drugs for
antianginal therapy (e.g., amlodipine, 5 to 10
mg/day orally, or diltiazem, 120 to 480 mg/day
orally as sustained release or divided doses) or
for control of heart rate in AF (e.g., diltiazem,
120 to 480 mg/day orally, or verapamil, 180 to
480 mg/day orally, as sustained release or in
divided doses)
Short-acting nifedipine should be avoided.
Hormone therapy with estrogen with or
without progestin is not begun after an
acute MI because it increases
thromboembolic risk and does not
prevent reinfarction
For women already receiving hormone
replacement, therapy should be
discontinued unless it is being given for
another compelling indication
Hypertension and diabetes mellitus must be assessed
and tightly controlled in patients after acute MI.
ACE inhibitors or -blockers as described earlier are usually
the first-choice therapies for hypertension, with ARBs
indicated when ACE inhibitors are not tolerated.
ACE inhibitors and ARBs also can reduce the long-term
complications of diabetes.

Antioxidant supplementation (e.g., vitamin E, vitamin


C) does not benefit patients after acute MI and is not
recommended. Folate therapy reduces homocyst(e)ine
levels, but it has not been effective in reducing clinical
events in large secondary prevention trials. Evidence
regarding fish oil supplements is insufficient to make
recommendations for or against them.

Antiarrhythmic drugs are not generally recommended


after acute MI, and class I antiarrhythmic agents can
increase the risk of sudden death.
Adaptation of Activity
Myocardial ischemia is caused by a
discrepancy between the demand of the
heart muscle for oxygen and the ability of
the coronary circulation to meet this demand
Most patients can be helped to understand
this concept and utilize it in the rational
programming of activity
Many tasks that ordinarily evoke angina may
be accomplished without symptoms simply by
reducing the speed at which they are
performed
Patients must appreciate the diurnal variation in
their tolerance of certain activities and should
reduce their energy requirements in the morning,
immediately after meals, and in cold or inclement
weather
On occasion, it may be necessary to recommend a
change in employment or residence to avoid
physical stress
However, with the exception of manual laborers,
most patients with IHD can continue to function
merely by allowing more time to complete each
task
In some patients, anger and
frustration may be the most
important factors precipitating
myocardial ischemia

If these cannot be avoided,


training in stress
management may be useful
A treadmill exercise test to determine the
approximate heart rate at which ischemic
ECG changes or symptoms develop may be
helpful in the development of a specific
exercise program
Physical conditioning usually improves the exercise
tolerance of patients with angina and exerts
substantial psychological benefits
A regular program of isotonic exercise that is within
the limits of each patient's threshold for the
development of angina pectoris and does not
exceed 80% of the heart rate associated with
ischemia on exercise testing should be strongly
encouraged
Based on the results of an exercise test, the number
of METS performed at the onset of ischemia can be
estimated and a practical exercise prescription can
be formulated to permit daily activities that will fall
below the ischemic threshold

S-ar putea să vă placă și