Cardiac Arrhythmia
Heart rhythm disturbances, fainting spells (نوبات الإغماء), and other medical problems which may
necessitate treatment with pacemakers and implantable(external) defibrillators are among the most
common conditions in medical practice. In many cases, afflicted individuals experience symptoms of
irregular or rapid heart beating within the chest, lightheadedness, dizziness, chest discomfort, and
blackout spellsنوبات فقدان) الوعي). Such symptoms cause considerable concern to patients and their
families and prevent individuals from enjoying a normal life and maintaining productive employment.
Heart Rhythm Disturbances
Under normal conditions the heart beats very regularly and its action is not perceptible (محسوس) to
most people. However, in many individuals the heart rhythm may be irregular, too fast, or too slow.
These problems may be the only manifestation of heart disease or they may occur as a result of
some other underlying heart problem (such as a previous heart attack). Not infrequently, it is the
heart rhythm disturbance, which causes the most symptoms. Dizziness, fatigue, blackout spells (نوبات
فقدان الوعي) or a sense of chest discomfort associated with rapid or irregular heart beating may result in
patients seeking medical attention.
In some cases the heart rhythm disturbance is quite innocent (حميد) and reassurance or minimal
treatment is adequate. In other cases, however, the heart rhythm disturbance may be life
threatening. In these cases, special medications, pacemakers, or implantable cardiac defibrillators
(special pacemakers designed to recognize life-threatening heart rhythm disturbances, and 'shock'
the rhythm back to normal) may be needed. In other instances, specialized techniques are available
to eliminate those irritable areas of the heart and essentially cure the problem.
The latter technique (often called 'ablation') is usually achieved with the use of special tubes which
are temporarily advanced through blood vessels to the heart in order to identify the abnormal site
and destroy it. This procedure is undertaken under local anesthetic and often the patient can go
home the next day. In a few cases, heart surgery is needed in order to solve the problem.
An expertise needed to diagnose heart rhythm problems, determine their severity, and provide
appropriate treatment after thorough discussion with the patient, their family and referring
physicians. Our goals are to listen, to inform, and to work with patients, their families and physicians
in providing the best possible solutions to troublesome heart rhythm problems.
Indicative Symptoms
Heart rhythm problems may occur in patients who have apparently normal hearts as well as in
individuals who have known or as yet undiagnosed heart problems. Symptoms of fatigue, dizziness,
chest discomforts, a sense of irregularity of the pulse, and blackout spells may be indicators of heart
rhythm disturbances. As medical treatments for various diseases prolong life, the number of
individuals with heart rhythm problems expands. Currently, heart rhythm disturbances are the most
important cause of sudden death.
Atrial Fibrillation
Atrial fibrillation is a rhythm emanating (انبعث) from the top chambers or atria of the heart. During
atrial fibrillation, there is a loss of coordinated contraction between the chambers of the heart and
the efficiency of the heart in general decreases by 10 to 30%. More than 10% of all people over 70
years of age will experience at least one episode of atrial fibrillation. Atrial fibrillation is associated
with increased risk of stroke, heart failure, and death. Researchers continue to study ways to both
prevent atrial fibrillation and to decrease the chances for life threatening complications.
We are currently involved in ongoing collaborative studies (دراسات مساندة) to determine the best therapy
for atrial fibrillation as well as studies to develop a new device which is capable of both pacing the
heart and delivering small amounts of drug into the chambers of the heart when atrial fibrillation
occurs. These latter studies are leading to a new and successful therapy for the treatment of atrial
fibrillation for a certain subset of patients. In addition, we continue to perform ongoing experiments
in the animal laboratory related to improved ways to rapidly terminate atrial fibrillation with a
combination of low energy shock therapy combined with drug therapies. Finally, we continue to
assess the potential efficacy of oral agents which may be of benefit in atrial fibrillation including clinical
testing of the drugs sotalol, amiodarone.
Studies on the Atrioventricular Node
Researchers have been interested in the way electrical impulses travel from the top of the heart, or
the atria, to the bottom of the heart, or the ventricle, for over two decades. Failure to conduct
electrical impulses properly can lead to loss of consciousness and sudden death. Both drug therapies
and pacemakers have been used to treat disorders of impulse conduction through the heart.
However, little is still known about the biochemical complex of the electrical network in the heart.
The atrioventricular nodal region of the heart is located in the middle of the complex cardiac
conduction system. This node situated between the atria and the ventricles, serves as a critical relay
station for electrical impulses. Researchers have developed novel techniques(أساليب غريبة ) to study
both the electrical and biochemical properties of this complex electrical region of the heart. Using
these techniques they have made a major breakthrough in understanding the way the central
nervous system controls impulse conduction through this portion of the heart.
Researchers have discovered that a family of membrane bound proteins, termed G proteins, play a
significant role in modulating atrioventricular conduction. The role of these G proteins in the electrical
system of the heart has previously been unknown. Based upon these new observations, researchers
intend to focus future efforts on ways to pharmacologically and genetically alter the functional
properties of these proteins in order to improve conduction through this portion of the cardiac
conduction system.
Calcium channel blockers:
Calcium antagonists (CA) might represent additional options in the treatment of chronic heart failure
(CHF) which accompanies arterial hypertension or coronary heart disease. These cardiovascular
diseases cause, in particular, the diastolic dysfunction of cardiac ventricles. At this time, there is no
specific therapy of diastolic dysfunction, but several drugs, among them CA, offer symptomatic relief
and may prevent progression of the disorder. This can be due to the positive effect on relaxation
and ventricular filling, the diminished coronary tone and better myocardial oxygen supply with
improvement both systolic and diastolic function, and the "unloading effect".
The major Haemodynamic alteration in most patients with chronic essential hypertension is an
increase in peripheral vascular resistance. This increase in the resistance results from an increase in
arteriolar smooth muscle tone that in turn is dependent upon the intracellular free calcium
concentration. Vascular smooth muscle has low intracellular calcium concentrations and smooth
muscle contraction depends upon an influx of extracellular calcium through calcium channels located
on the cell membrane. The calcium channel blockers inhibit the movement of extracellular calcium
through these calcium channels and result in arteriolar dilation and a decrease in blood pressure.
It has been proposed that elderly and black patients have greater blood pressure responses to
calcium channel blockers than younger white patients. This has not been confirmed in all clinical trials.
Calcium channel blockers also appear to slow the progression of renal impairment. The exact
mechanism for this action is still controversial. Some studies have found that calcium channel
blockers dilate the afferent arteriole, which would increase glomerular pressure. Other studies
suggest equal vasodilatory effect on the afferent and efferent arterioles, which would decrease
intraglomeriolar pressure
Diltiazem is the drug belong to Type 1 Ca++-blocker of the group called benzothiazepines, other
type of group one is called Diphynylalkylamines including verapamil and it’s congeners, tiapamil and
gallopamil. All these agents have similar effects on myocardial and peripheral tissue. They slow
conduction across the (AV) node and prolong the refractoriness. These drugs can depress
myocardial contractility, they are moderate peripheral vasodilators, and they are selective because
they affect the calcium channels in the myocardium.
Ventricular tackycardia
Defined as three or more ventricular beats occurring at a rate of 120 b.p.m. or more due to a
premature ventricular contractions. Examination revealed a pulse rate of 120-220 b.p.m. Usually
there are clinical signs of atrioventricular dissociation. The ECG shows a rapid ventricular rhythm with
broad, abnormal QRS complexes. Dissociated P wave activity may be seen.
Many common factors which cause ventricular arrhythmias are ischemia, presence of organic heart
disease, exercise, metabolic or electrolyte imbalance, drugs (digitalis, sympathomimitic amines,
antiarrhythmias), it is essential to remove and treat the cause.
Diltiazem has a negligible effect on the effective refractory period of the ventricle.
Supraventricular tackycardia
Tackycardia other than the ventricular tackycardia, which include many Arrhythmias and the most
common, is atrial fibrillation and atrial flutter.
Inhibition of calcium entrance into the myocardium prolonged the refractory period of atrioventricular
node. Diltiazem decrease heartbeat and so sinus rhythm from 173 to 115beats/min. and 12mmHg in
some studies.
Atrial fibrillation
Atrial fibrillation commonly caused by a raised atrial pressure, increased atrial muscle mass, atrial
fibrosis, or inflammation of the atrium.
Atrial fibrillation is continuous, rapid activation of the atria. Alcohol toxicity and thyrotoxicosis may
precipitate this condition. ECG shows no clear P wave, QRS rhythm is rapid and irregular.
Causes include myocardial infarction, valvular heart disease, coronary artery disease, cardiac
infection, CHF, thyrotoxicosis.
Oral Diltiazem 60 to 90 mg 4 times daily induce a beneficial effect in slowing the ventricular rate in
patients with atrial fibrillation or flutter, and also when used with digoxin.
Atrial flutter
This is a rhythm disturbance that is usually associated with organic heart disease. Impulses rate is
about 220 to 350 b.p.m.
Causes include myocardial infarction, valvular heart disease, coronary artery disease, cardiac
infection, CHF, thyrotoxicosis.
Coronary artery constriction induced by catecholamine release may contribute to the development of
angina during exertion in some patients with coronary stenosis (الشريان التاجيتضيق ). Diltiazem relaxes the
contraction induced by both 1- and 2- adrenocepter agonists, thus a beneficial effect on
coronary artery tone and exercise tolerance would be predicted.
Heart rhythm disturbances, fainting spells (نوبات الإغماء), and other medical problems which may
necessitate treatment with pacemakers and implantable(external) defibrillators are among the most
common conditions in medical practice. In many cases, afflicted individuals experience symptoms of
irregular or rapid heart beating within the chest, lightheadedness, dizziness, chest discomfort, and
blackout spellsنوبات فقدان) الوعي). Such symptoms cause considerable concern to patients and their
families and prevent individuals from enjoying a normal life and maintaining productive employment.
Heart Rhythm Disturbances
Under normal conditions the heart beats very regularly and its action is not perceptible (محسوس) to
most people. However, in many individuals the heart rhythm may be irregular, too fast, or too slow.
These problems may be the only manifestation of heart disease or they may occur as a result of
some other underlying heart problem (such as a previous heart attack). Not infrequently, it is the
heart rhythm disturbance, which causes the most symptoms. Dizziness, fatigue, blackout spells (نوبات
فقدان الوعي) or a sense of chest discomfort associated with rapid or irregular heart beating may result in
patients seeking medical attention.
In some cases the heart rhythm disturbance is quite innocent (حميد) and reassurance or minimal
treatment is adequate. In other cases, however, the heart rhythm disturbance may be life
threatening. In these cases, special medications, pacemakers, or implantable cardiac defibrillators
(special pacemakers designed to recognize life-threatening heart rhythm disturbances, and 'shock'
the rhythm back to normal) may be needed. In other instances, specialized techniques are available
to eliminate those irritable areas of the heart and essentially cure the problem.
The latter technique (often called 'ablation') is usually achieved with the use of special tubes which
are temporarily advanced through blood vessels to the heart in order to identify the abnormal site
and destroy it. This procedure is undertaken under local anesthetic and often the patient can go
home the next day. In a few cases, heart surgery is needed in order to solve the problem.
An expertise needed to diagnose heart rhythm problems, determine their severity, and provide
appropriate treatment after thorough discussion with the patient, their family and referring
physicians. Our goals are to listen, to inform, and to work with patients, their families and physicians
in providing the best possible solutions to troublesome heart rhythm problems.
Indicative Symptoms
Heart rhythm problems may occur in patients who have apparently normal hearts as well as in
individuals who have known or as yet undiagnosed heart problems. Symptoms of fatigue, dizziness,
chest discomforts, a sense of irregularity of the pulse, and blackout spells may be indicators of heart
rhythm disturbances. As medical treatments for various diseases prolong life, the number of
individuals with heart rhythm problems expands. Currently, heart rhythm disturbances are the most
important cause of sudden death.
Atrial Fibrillation
Atrial fibrillation is a rhythm emanating (انبعث) from the top chambers or atria of the heart. During
atrial fibrillation, there is a loss of coordinated contraction between the chambers of the heart and
the efficiency of the heart in general decreases by 10 to 30%. More than 10% of all people over 70
years of age will experience at least one episode of atrial fibrillation. Atrial fibrillation is associated
with increased risk of stroke, heart failure, and death. Researchers continue to study ways to both
prevent atrial fibrillation and to decrease the chances for life threatening complications.
We are currently involved in ongoing collaborative studies (دراسات مساندة) to determine the best therapy
for atrial fibrillation as well as studies to develop a new device which is capable of both pacing the
heart and delivering small amounts of drug into the chambers of the heart when atrial fibrillation
occurs. These latter studies are leading to a new and successful therapy for the treatment of atrial
fibrillation for a certain subset of patients. In addition, we continue to perform ongoing experiments
in the animal laboratory related to improved ways to rapidly terminate atrial fibrillation with a
combination of low energy shock therapy combined with drug therapies. Finally, we continue to
assess the potential efficacy of oral agents which may be of benefit in atrial fibrillation including clinical
testing of the drugs sotalol, amiodarone.
Studies on the Atrioventricular Node
Researchers have been interested in the way electrical impulses travel from the top of the heart, or
the atria, to the bottom of the heart, or the ventricle, for over two decades. Failure to conduct
electrical impulses properly can lead to loss of consciousness and sudden death. Both drug therapies
and pacemakers have been used to treat disorders of impulse conduction through the heart.
However, little is still known about the biochemical complex of the electrical network in the heart.
The atrioventricular nodal region of the heart is located in the middle of the complex cardiac
conduction system. This node situated between the atria and the ventricles, serves as a critical relay
station for electrical impulses. Researchers have developed novel techniques(أساليب غريبة ) to study
both the electrical and biochemical properties of this complex electrical region of the heart. Using
these techniques they have made a major breakthrough in understanding the way the central
nervous system controls impulse conduction through this portion of the heart.
Researchers have discovered that a family of membrane bound proteins, termed G proteins, play a
significant role in modulating atrioventricular conduction. The role of these G proteins in the electrical
system of the heart has previously been unknown. Based upon these new observations, researchers
intend to focus future efforts on ways to pharmacologically and genetically alter the functional
properties of these proteins in order to improve conduction through this portion of the cardiac
conduction system.
Calcium channel blockers:
Calcium antagonists (CA) might represent additional options in the treatment of chronic heart failure
(CHF) which accompanies arterial hypertension or coronary heart disease. These cardiovascular
diseases cause, in particular, the diastolic dysfunction of cardiac ventricles. At this time, there is no
specific therapy of diastolic dysfunction, but several drugs, among them CA, offer symptomatic relief
and may prevent progression of the disorder. This can be due to the positive effect on relaxation
and ventricular filling, the diminished coronary tone and better myocardial oxygen supply with
improvement both systolic and diastolic function, and the "unloading effect".
The major Haemodynamic alteration in most patients with chronic essential hypertension is an
increase in peripheral vascular resistance. This increase in the resistance results from an increase in
arteriolar smooth muscle tone that in turn is dependent upon the intracellular free calcium
concentration. Vascular smooth muscle has low intracellular calcium concentrations and smooth
muscle contraction depends upon an influx of extracellular calcium through calcium channels located
on the cell membrane. The calcium channel blockers inhibit the movement of extracellular calcium
through these calcium channels and result in arteriolar dilation and a decrease in blood pressure.
It has been proposed that elderly and black patients have greater blood pressure responses to
calcium channel blockers than younger white patients. This has not been confirmed in all clinical trials.
Calcium channel blockers also appear to slow the progression of renal impairment. The exact
mechanism for this action is still controversial. Some studies have found that calcium channel
blockers dilate the afferent arteriole, which would increase glomerular pressure. Other studies
suggest equal vasodilatory effect on the afferent and efferent arterioles, which would decrease
intraglomeriolar pressure
Diltiazem is the drug belong to Type 1 Ca++-blocker of the group called benzothiazepines, other
type of group one is called Diphynylalkylamines including verapamil and it’s congeners, tiapamil and
gallopamil. All these agents have similar effects on myocardial and peripheral tissue. They slow
conduction across the (AV) node and prolong the refractoriness. These drugs can depress
myocardial contractility, they are moderate peripheral vasodilators, and they are selective because
they affect the calcium channels in the myocardium.
Ventricular tackycardia
Defined as three or more ventricular beats occurring at a rate of 120 b.p.m. or more due to a
premature ventricular contractions. Examination revealed a pulse rate of 120-220 b.p.m. Usually
there are clinical signs of atrioventricular dissociation. The ECG shows a rapid ventricular rhythm with
broad, abnormal QRS complexes. Dissociated P wave activity may be seen.
Many common factors which cause ventricular arrhythmias are ischemia, presence of organic heart
disease, exercise, metabolic or electrolyte imbalance, drugs (digitalis, sympathomimitic amines,
antiarrhythmias), it is essential to remove and treat the cause.
Diltiazem has a negligible effect on the effective refractory period of the ventricle.
Supraventricular tackycardia
Tackycardia other than the ventricular tackycardia, which include many Arrhythmias and the most
common, is atrial fibrillation and atrial flutter.
Inhibition of calcium entrance into the myocardium prolonged the refractory period of atrioventricular
node. Diltiazem decrease heartbeat and so sinus rhythm from 173 to 115beats/min. and 12mmHg in
some studies.
Atrial fibrillation
Atrial fibrillation commonly caused by a raised atrial pressure, increased atrial muscle mass, atrial
fibrosis, or inflammation of the atrium.
Atrial fibrillation is continuous, rapid activation of the atria. Alcohol toxicity and thyrotoxicosis may
precipitate this condition. ECG shows no clear P wave, QRS rhythm is rapid and irregular.
Causes include myocardial infarction, valvular heart disease, coronary artery disease, cardiac
infection, CHF, thyrotoxicosis.
Oral Diltiazem 60 to 90 mg 4 times daily induce a beneficial effect in slowing the ventricular rate in
patients with atrial fibrillation or flutter, and also when used with digoxin.
Atrial flutter
This is a rhythm disturbance that is usually associated with organic heart disease. Impulses rate is
about 220 to 350 b.p.m.
Causes include myocardial infarction, valvular heart disease, coronary artery disease, cardiac
infection, CHF, thyrotoxicosis.
Coronary artery constriction induced by catecholamine release may contribute to the development of
angina during exertion in some patients with coronary stenosis (الشريان التاجيتضيق ). Diltiazem relaxes the
contraction induced by both 1- and 2- adrenocepter agonists, thus a beneficial effect on
coronary artery tone and exercise tolerance would be predicted.
Cardiovascular Diseases
 |  |
Cardiac Arrhymia