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CORONARY ARTERY
DISEASE
PRESENTED BY
DR TASNEEM MALIK
MPH3RD SEMESTER
DUHS KHI
JAN-2016
 PATHOPHYSIOLOGY
 GENETIC FACTORS
 RECENT TREATMENT IN GENETICS
 Genetic factors involved in:
 Autosomal recessive disorder
 2q34-37 and3q26-27
 2q locus have many candidate genes
including
 UGT1A1(responsible for in billirubin level in
Gilbert syndrome).
 Recently 2658 affected sib pairs found
Linkage to a large region 36 MB on
chromosome 17 having 300 genes many of
which are candidates based on function or
epresion.
 FH
 Autosomal inherited
disorder.
 Hetrozygous for a
mutation in LDLR
on cell surface.
 Responsible for
increased risk for
early CAD
 MEF2A
 No certain link
Treatment of Coronary Artery Disease
The prevalence of coronary artery disease is on the rise and in
2009 accounted for 1 of every 6 deaths in the United
States. Long-term survival of patients with coronary disease has
increased because of advances treatments with following drugs
• Lipid lowering agents
•DIETRY CHANGES
•INCREASE VEGETABLES
•DECREASE MEAT
Gene Therapy for the Treatment of Coronary Artery Disease
The prevalence of coronary artery disease is on the rise and in 2009
accounted for 1 of every 6 deaths in the United States. Long-term
survival of patients with coronary disease has increased because of
advances in pharmacologic and revascularization techniques.
However, a group of patients who are refractory to conventional
therapy has emerged.
These patients suffer from severe angina pectoris despite maximal
medical therapy and are no longer treatable with percutaneous
coronary intervention or coronary artery bypass graft surgery. An
alternative treatment option is being developed, termed therapeutic
angiogenesis.
The therapy involves administration of genes for
angiogenic growth factors to augment collateral vessel
development. Preclinical successes led to the hope that this strategy
would provide a solution to the ongoing clinical problem.
A series of lackluster clinical trials has dimmed this
hope. A widespread conclusion of these
investigations is that angiogenesis is a complex
mechanism requiring precise timing of multiple
growth factors acting on receptors to stimulate and
then sustain new vessel growth.
Coronary artery disease

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Coronary artery disease

  • 1. CORONARY ARTERY DISEASE PRESENTED BY DR TASNEEM MALIK MPH3RD SEMESTER DUHS KHI JAN-2016
  • 2.  PATHOPHYSIOLOGY  GENETIC FACTORS  RECENT TREATMENT IN GENETICS
  • 3.
  • 4.
  • 5.  Genetic factors involved in:  Autosomal recessive disorder  2q34-37 and3q26-27  2q locus have many candidate genes including  UGT1A1(responsible for in billirubin level in Gilbert syndrome).  Recently 2658 affected sib pairs found Linkage to a large region 36 MB on chromosome 17 having 300 genes many of which are candidates based on function or epresion.
  • 6.  FH  Autosomal inherited disorder.  Hetrozygous for a mutation in LDLR on cell surface.  Responsible for increased risk for early CAD  MEF2A  No certain link
  • 7. Treatment of Coronary Artery Disease The prevalence of coronary artery disease is on the rise and in 2009 accounted for 1 of every 6 deaths in the United States. Long-term survival of patients with coronary disease has increased because of advances treatments with following drugs • Lipid lowering agents •DIETRY CHANGES •INCREASE VEGETABLES •DECREASE MEAT
  • 8.
  • 9. Gene Therapy for the Treatment of Coronary Artery Disease The prevalence of coronary artery disease is on the rise and in 2009 accounted for 1 of every 6 deaths in the United States. Long-term survival of patients with coronary disease has increased because of advances in pharmacologic and revascularization techniques. However, a group of patients who are refractory to conventional therapy has emerged. These patients suffer from severe angina pectoris despite maximal medical therapy and are no longer treatable with percutaneous coronary intervention or coronary artery bypass graft surgery. An alternative treatment option is being developed, termed therapeutic angiogenesis. The therapy involves administration of genes for angiogenic growth factors to augment collateral vessel development. Preclinical successes led to the hope that this strategy would provide a solution to the ongoing clinical problem.
  • 10. A series of lackluster clinical trials has dimmed this hope. A widespread conclusion of these investigations is that angiogenesis is a complex mechanism requiring precise timing of multiple growth factors acting on receptors to stimulate and then sustain new vessel growth.