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Interventional CardiologyWhat you know!What you should know!What you think you know!

Jorge Alvarez M.D., F.A.C.C.,F.S.C.A.I.

Lets Start by Taking a Look Inside First.

AtherothrombosisCAD is a progressive disease, but the speed of progression varies tremendously, even among persons with similar risk factor levels and among arteries within the same person. The reasons for this diversity in disease progression have not been identified, but both persons and arteries probably differ in their susceptibility to atherogenic and thrombogenic stimuli.Serial angiographic and pathoanatomical observations indicate that progression of CAD involves two distinct processes 1st a fixed and hardly reversible process that causes gradual luminal narrowing slowly over decades (atherosclerosis) 2nd a dynamic and potentially reversible process that punctuates the slow progression in a sudden and unpredictable way, causing rapid coronary occlusion (thrombosis).

Cross-sectioned coronary artery illustrating a mature collagen-rich atherosclerotic plaque (collagen is blue) containing a lipid-rich core (asterisk) that luminally is covered by a thick fibrous cap.

Thus, symptomatic coronary lesions contain a variable mix of chronic atherosclerosis and acute thrombosis, but because the exact nature of the mix is unknown in the individual patient, the term atherothrombosis is frequently used. Generally, atherosclerosis predominates in lesions responsible for chronic stable angina, whereas thrombosis constitutes the critical component of culprit lesions responsible for the ACSs.

Cross-sectioned arterial bifurcation illustrating a collagen-rich (blue-stained) plaque in the circumflex branch (left), and a lipid-rich and ruptured plaque with a nonocclusive thrombosis superimposed in the obtuse branch (right).

B2O = Birth to Occlusion time line

ST Elevation Myocardial Infarction

Patients Transported by EMS after Calling 911

Why Time Matters

J Am Coll Cardiol 2006;47:2180–6

Time to primary PCI is strongly associated with mortality risk and is important regardless oftime from symptom onset to presentation and regardless of baseline risk of mortality. Efforts to shorten door-to-balloon time should apply to all patients.

What if they present late?

Mean reduction in door-to-balloon times by strategy

8.6Having staff in ED and cath lab use and receive real-time feedback

14.6Having an attending cardiologist always on site

19.3Expecting staff to arrive at cath lab within 20 minutes after page

15.4Having the ED activate the cath lab while patient still en route

13.8Having a single call to a central page operator activate cath lab

8.2Having emergency medicine physicians activate the cath lab

Mean reduction in door-to-balloon time (min)

Strategy

This is A Heart Attack

The Past

What is Magnum PI doing in the cath lab?

The First Angioplasty

Then There Were Stents

How Does It Work?

Vincent Van Gogh

Restenosis

Drug-Eluting Stents

How it WorksPablo Picasso

They Work Very Well

They Work To Well!

This is why we need antiplatelet therapy for 1 year

Future Stent Designs

Bioabsorbable Stents

We are just getting Started

Holes in the Heart

What you see with Angiography

is not always the whole picture

Intermediate LAD Stenosis in a patient with Sxs and a Positive ETT

Intermediate LAD Stenosis in a patient with Sxs and a Positive ETT

VH versus Grayscale IVUS

Vincent Van Gogh

What is PAD?Peripheral Artery Disease (PAD)

Occurs when arteries in the leg become narrowed or clogged with plaque, which can result in:

Decreased blood flow Pain and discomfortLimited mobility

If left untreated, PAD can lead to Critical Limb Ischemia (CLI)

CLI occurs when not enough blood is delivered to the leg to keep the tissue alive, often resulting in amputation.

Note:Arteries are blood vessels traveling away from the heart. Veins are blood vessels traveling to the heart.

ArterialBlood Flow

PAD Population

4.6 4.8

8.9

12 12.6

17.0

0

246

8

10121416

18

Mill

ions

StrokeCongestive

Heart Failure Cancer PADCoronary

Artery Disease Diabetes

1. Endovascular Today; Feb. 04. Vol. 3., #2

SilverHawk® Plaque Excision

What is SilverHawk Plaque Excision?A minimally invasive procedure to remove plaque from the arteries

How does it work?It removes obstructing plaque from arteries by gently scooping it out

Alternative to Amputation and surgical options such as Leg Artery BypassComparable recovery time to other endovascular treatments

What does Plaque look like?

Actual plaque, removed from PAD patients

Vincent Van Gogh

Patient History:• 80-year-old male• Ex-smoker• History of Coronary Artery Disease, High Blood Sugar, Prior Bypass Surgery• Non-healing wound and tissue loss on his left great toenail

Before Procedure

Blockage

60 days post Procedure

BlockageRemoved

Case Study Examples

Patient History:• 64-year-old male• Critical Limb Ischemia • History of Coronary Artery Disease • High Cholesterol

Pre

Before Procedure

Blockage

Post

45 days post Procedure

Blockage Removed

Case Study Examples

Unable to walk for 1 block without severe Buttock Pain

Kissing stents in the aortic bifurcation

Pablo Picasso

Not just for the legs anymore

On the Horizon?

Left Atrial Appendage occlusion

Valvular Heart Disease

Mitral Valve Clip

RV Infarct

Complications

1) Cardiogenic shock2) RV infarction/ischemia 3) Ischemic mitral valve regurgitation (MR)4) Ventricular septal defect (VSD)5) LV free wall rupture.

Questions

Which of the following are related to development of plaque rupture?

A. Inflammation. B. Cholesterol content. C. Oxidized LDL. D. All of the above.

Questions

Which of the following are related to development of plaque rupture?

A. Inflammation. B. Cholesterol content. C. Oxidized LDL. D. All of the above.

What size plaques lead to MI, measured in baseline % stenosis pre-MI?

A. 30-50%. B. 51-70%.C. 71-90%. D. >90%.

What size plaques lead to MI, measured in baseline % stenosis pre-MI?

A. 30-50%.B. 51-70%.C. 71-90%. D. >90%.

Which feature does not characterize a vulnerable plaque?

A. Soft lipid rich core.B. Macrophage infiltration of the shoulder region.C. Thick fibrous cap.D. Few smooth muscle cells in fibrous cap.

Which feature does not characterize a vulnerable plaque?

A. Soft lipid rich core.B. Macrophage infiltration of the shoulder region.C. Thick fibrous cap.D. Few smooth muscle cells in fibrous cap.

Which factor does not contribute to plaque destabilization?

A. High serum cholesterol and LDL levels.B. Decreased collagen synthesis.C. Increased collagen synthesis.D. Increased collagen degradation.

Which factor does not contribute to plaque destabilization?

A. High serum cholesterol and LDL levels.B. Decreased collagen synthesis.C. Increased collagen synthesis.D. Increased collagen degradation.

A 75-year-old male presented with four hours of chest pain and ST-segment elevation in ECG leads II, III, aVF, and V5-6. He received tenecteplase in the ER, with resolution of the chest pain and ST-segment changes. Upon admission to the critical ICU, the patient was hemodynamically stable. TTE on hospital day two revealed normal LV systolic size and function, with no significant valvular abnormalities. On hospital day three, he developed acute hypotension, tachycardia, and hypoxemia, and was noted on exam to have pulmonary rales, and a new holosystolic murmur along the left parasternal border. What is your diagnosis?

A. Ventricular septal rupture.B. Acute mitral regurgitation due to papillary muscle rupture.C. Free wall rupture and tamponade.D. RV infarct.

A 75-year-old male presented with four hours of chest pain and ST-segment elevation in ECG leads II, III, aVF, and V5-6. He received tenecteplase in the ER, with resolution of the chest pain and ST-segment changes. Upon admission to the critical ICU, the patient was hemodynamically stable. TTE on hospital day two revealed normal LV systolic size and function, with no significant valvularabnormalities. On hospital day three, he developed acute hypotension, tachycardia, and hypoxemia, and was noted on exam to have pulmonary rales, and a new holosystolic murmur along the left parasternal border. What is your diagnosis?

A. Ventricular septal rupture.B. Acute mitral regurgitation due to papillary muscle rupture.C. Free wall rupture and tamponade.D. RV infarct.

A 60-year-old female presented to the ER with one-day history of intense left-sided chest pressure, 10 out of 10, associated with nausea, vomiting, and diaphoresis. Vital signs were: BP 141/91, pulse 80. Physical exam revealed bilateral carotid bruits, no elevated jugular venous pressure. Heart exam showed S1 S2 with S4, no murmur, and clear lungs. Initial troponin I was 1.04 (peaked at 35 ng/dl). 2D echo showed 35% EF with postero-inferior hypokinesis and no major valvular heart disease. The patient had more chest pain on day 4 and was referred for heart catheterization. Cardiac cath revealed 90% lesion in the mid circumflex artery and nonobstructive disease in the LAD artery and the right coronary artery. Awaiting angioplasty of the circumflex artery, the patient suddenly became pulseless and unresponsive. ECG showed sinus tachycardia. CPR was initiated for pulseless electrical activity. What is the cause of the pulseless electrical activity arrest?

A. Ventricular septal rupture.B. Acute mitral regurgitation due to papillary muscle rupture.C. Free wall rupture and tamponade.D. RV infarct.

A 60-year-old female presented to the ER with one-day history of intense left-sided chest pressure, 10 out of 10, associated with nausea, vomiting, and diaphoresis. Vital signs were: BP 141/91, pulse 80. Physical exam revealed bilateral carotid bruits, no elevated jugular venous pressure. Heart exam showed S1 S2 with S4, no murmur, and clear lungs. Initial troponin I was 1.04 (peaked at 35 ng/dl). 2D echo showed 35% EF with postero-inferior hypokinesis and no major valvular heart disease. The patient had more chest pain on day 4 and was referred for heart catheterization. Cardiac cath revealed 90% lesion in the mid circumflex artery and nonobstructive disease in the LAD artery and the right coronary artery. Awaiting angioplasty of the circumflex artery, the patient suddenly became pulseless and unresponsive. ECG showed sinus tachycardia. CPR was initiated for pulseless electrical activity. What is the cause of the pulseless electrical activity arrest?

A. Ventricular septal rupture.B. Acute mitral regurgitation due to papillary muscle rupture.C. Free wall rupture and tamponade.D. RV infarct.

Which of the following characteristics would you expect with acute inferior STEMI with severe RV ischemia?

A. Critical stenosis of the left main or proximal LAD coronary artery.B. Hypotension, elevated jugular venous pressure, and clear lung exam.C. Pulmonary artery capillary wedge pressure >2x the central venous pressure.D. Permanent stunning and akinesis of the RV myocardium.E. Paradoxical increase in systemic BP postnitroglycerine administration. and emergent surgical repair.

Which of the following characteristics would you expect with acute inferior STEMI with severe RV ischemia?

A. Critical stenosis of the left main or proximal LAD coronary artery.B. Hypotension, elevated jugular venous pressure, and clear lung exam.C. Pulmonary artery capillary wedge pressure >2x the central venous pressure.D. Permanent stunning and akinesis of the RV myocardium.E. Paradoxical increase in systemic BP postnitroglycerine administration. and emergent surgical repair.

Thank You