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 Angina is experienced as a heavy, pressing
substernal discomfort (rarely described as a
"pain"), often radiating to the left shoulder, flexor
aspect of the left arm, jaw, or epigastrium.
 Angina is the result of myocardial ischemia
caused by an imbalance between myocardial
blood supply and oxygen demand.
 Angina isn't a disease; it's a symptom of an
underlying coronary heart disease(CHD).

(Brunton et al, 2011; AHA,2014)


Angina

variant
Stable Unstabel Micro-
(Prinz-
Angina Angina vascular
metal's)

Chronic Acute
Coronary Coronary
Disease Disease (AHA, 2014; Aaronson et al,2000)
Stable • It occurs when the heart is working
harder than usual. S
Angina • Table angina has a regular pattern.

• Unstable angina doesn't follow a


Unstable pattern.
• Unstable angina can occur with or
Angina without physical exertion, and rest or
medicine may not relieve the pain

(Aaronson et al,2000 ;AHA, 2014;)


(Newby et al, 2010)
• Variant angina is rare.
Variant • A spasm in a coronary artery causes this
(Prinzmetal's) type of angina.

• This is heart disease that affects the


heart’s smallest coronary arteries and is
Mikrovaskular more likely to affect women than men.
• Coronary MVD also is called cardiac
syndrome X and non-obstructive CHD.

(Aaronson et al,2000 ;AHA, 2014;)


Chronic Stable Angina/Angina Pectoris:
 Coronary Artery Disease(CAD):
atherosclerotic, congenital anomalies, emboli, arteritis, or
dissection may cause ischemia or infarction.
 Severe Myocardial Hypertrophy,
 Severe Aortic Valve Stenosis
 Increased Metabolic Demands
hyperthyroidism, marked anemia, or paroxysmal tachycardias with
rapid ventricular rates

(Bashore et al , 2015)
 ECG
Effects of increasing the heart
rate by atrial pacing in a patient
with typical stable angina.
Pacing stress caused a rapid
switch from lactate uptake to
lactate production,
a drop in the ST segment of
the electrocardiogram, and
chest pain.
Cessation of pacing resulted in
a rapid reversal from lactate
production back to net uptake,
elimination of pain, and a return
to a normal ST segment.
LVEDP, left ventricular end-
diastolic pressure

(Anderson et al, 2007)


(Crawford, 2009)
Therapy Mechanism

Aggravating Identified and treated Factors. [hypertension, LV Decrease Ox


Factors failure, arrhythmia (usually tachycardias), Demand
strenuous activity, cold temperatures, and
emotional states.]
Nitrogliserin- increased coronary vasomotor tone and dilate Increase Ox
Long-Acting coronary obstructions. Supply
Nitrates Venodilation, reducing preload and decreasing Decrease Ox
left ventricular enddiastolic volume. Demand
Calcium Coronary vasodilation, specifically on the Increase Ox
Channel smaller coronary Supply
Blockers Afterload reduction as a result of decreased Decrease Ox
blood pressure. Demand
Therapy of vasospasm
β-Adrenergic Reduction in myocardial consumption, heart rate, Decrease Ox
Blockers blood pressure, and myocardial contractility Demand

(Antman&Sabatine,2013)
Therapy Mechanism

Ranolazine specific inhibitor of late sodium current, Ion homeostasis


reduces sodium overload and hence
ameliorates disturbed ion homeostasis.
Alternative Patients who do not respond to one class of (β-blocker +
and antianginal medication often respond to nitrate) or
Combination another. It may, therefore, be worthwhile to (β-blocker +
Therapies use an alternative agent before progressing CCB)
to combinations.
Platelet- Several studies have demonstrated the Aspirin
Inhibiting benefit of antiplatelet drugs for patients Clopidogrel
Agents with stable and unstable vascular disease.
Risk This approach, with a particular focus on
Reduction statin treatment, treating hypertension,
stopping smoking, and exercise and weight
control

(Antman&Sabatine,2013)
Therapy Mechanism

Revasculari Indication: Coronary


zation (1) Patients with unacceptable symptoms artery bypass
despite medical therapy to its tolerable limits. grafting
(2) Patients with left main coronary artery
stenosis > 50% with or without symptoms. Percutaneous
(3) Patients with three-vessel disease with LV coronary
dysfunction (EF < 50% or previous transmural intervention
infarction). including
(4) Patients with unstable angina who after stenting—
symptom control by medical therapy continue to
exhibit ischemia on exercise testing or
monitoring.
(5) Post-myocardial infarction patients with
continuing angina or severe ischemia on
noninvasive testing.

(Antman&Sabatine,2013)
Therapy Mechanism

Mechanical entails repetitive inflation of a high-pressure


Extracorporeal chamber surrounding the lower half of the
Counterpulsation body during the diastolic phase of the cardiac
cycle for daily 1-hour sessions over a period of
7 weeks.
Randomized trials have shown that ECP
reduces angina, improves exercise tolerance,
and can reduce symptoms of heart failure.
Neuromodulation Spinal cord stimulation can be used to relieve
chronic refractory angina. Spinal cord
stimulators are subcutaneously
implantable via a minimally invasive
procedure under local anesthesia

(Antman&Sabatine,2013)
(Pappano &wier , 2013)
 Two larger phase three studies have examined the efficacy
of sustained release ranolazine in patients with chronic
stable angina.
 MARISA (Monotherapy Assessment of Ranolazine In
Stable Angina)
showed that ranolazine monotherapy significantly improved
exercise performance in patients with stable angina. This
was true for exercise duration, time to angina and time to 1
mm ST segment depression. More specifically, 70% of
patients in the placebo group stopped their exercise test
because of angina as compared to only 52% in the
ranolazine group (1.5 g bidaily).
Hasenfuss and Maier ,2007
 CARISA (Combination Assessment of Ranolazine in
Stable Angina)
CARISA improved peak and trough exercise duration, time
to angina and time to 1 mm ST depression. These effects
were sustained through a 12-week treatment. Also
ranolazine reduced the number of angina attacks from a
baseline of 4.5 per week to 2.1 per week for ranolazine (1 g
bidaily) compared to 3.3 per week for placebo. Most
importantly, the anti-anginal effects of ranolazine in MARISA
and CARISA occurred without clinical meaningful changes
in heart rate or blood pressure

Hasenfuss and Maier ,2007


 Moreover, calcium overload subsequent to
disturbed sodium homeostasis may also be a
major pathophysiological factor in diastolic
heart failure.
 Therefore we speculate that in diastolic
heart failure due to disturbed
sodium/calcium homeostasis, ranolazine
may represent a new attractive treatment
option.
References
Aaronson,P.I., Ward, J.P.T., Wiener, C.M.,Schulman, S.P., Gill, J.S.2007.
The Cardiovascular System at a Glance. Malden: Blackwell Science Ltd.

American Heart Association (AHA).2014. Angina (Chest


Pain).http://www.heart.org/HEARTORG/Conditions/HeartAttack/Symptoms
DiagnosisofHeartAttack/Angina-Chest-
Pain_UCM_450308_Article.jsp(Accessed 2015-03-03)

Antman, E.M., Sabatine, M.S. 2013.Cardiovascular Therapeutics: A


Companion to Braunwald's Heart Disease 4th Ed. Philadelphia:Elsivier

Antman, E.M., Selwyn, A.P., Braunwald,E., Loscalzo, J. 2010. Ischemic


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References
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Pharmacological Basis of Therapeutics 12th Ed. McGraw-Hill Companies
Inc: China

Crawford, M.H. 2009.Chronic Ischemic Heart Disease. In: Current


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Press Inc. P 174

Newby, D.E., Grubb,N.R.,Bradbury,A. 2010. Colledge, N.R., Walker,


B.R.,Ralston,S.H (Eds) Cardiovascular disease. In: Davidson's Principles
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References
Trujillo, T.C. and Nolan, P.E. 2013. Chronic Stable Angina. In: Alldredge,
B.K., Corelli,R.L., Guglielmo B.J., Jacobson, P.A.,Kradjan,
W.A.,Williams,B.R. (eds). Koda-Kimble & Young's Applied Therapeutics :
The Clinical Use of Drugs. Lippincott Williams & wilkins, Wolters Kluwer:
Philadelphia,USA

Pappano,A.J., Wier W.G. 2013. Cardiocaskular Physiology 10th


Ed.Philadelphia: Elsivier inc. pp:233