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Posts Tagged ‘intra coronary pressure’

Thousands of  coronary angiograms are done every day. Cardiologist no longer get excited to see exotic coronary lesions .Still , some images can be striking and dramatic. Here is an angiogram from a middle aged man  with stable angina  , who was  one among the routine early morning diagnostic studies  in our cath lab.

Who chopped the neck of this LAD ?

How this man was able to fill up the distal LAD almost completely? (With a complete cut off  right in the neck of LAD )

Are you sure there is antegrade flow ?

Do you get any clue ?

  • Can a trickle of  ante grade flow  sustain  a  TIMI 3 FLOW  ?
  • Or is it a  very efficient  instant collaterals  from LCX ?

Yes . The first one is right . An almost invisible antegrade channel  doing a exemplary job !

How is it possible ?

Realize an important fact . The distal flow beyond an obstruction  is not primarily dependent on degree of obstruction but the status of the distal vascular  bed .  If it is normal  even a hair-line patency  can  profusely perfuse the distal myocardial segment. This is what is happening to this man with a stable angina and perfectly normal micro vascular bed.

Lessens  from this Image.

Do not get fooled by the lay man’s logic. Realise there is  no simple relation  between  the degree of obstruction and degree of  blood flow impediment.It can be linear , curvilinear , or even inverse depending upon   the evolution and timing of obstruction  ,  number of lesions , presence or absence of collateral support , finally and  most importantly  the integrity of microvascular bed .

The  distal vascular bed drops its resistance drastically  once it senses  the problem in  proximal segment . This is based on Bernoulli principle and  is akin to how a  garden hose pipe  can simply increase  the velocity  by tightening the nozzle.*


* The garden hose analogy is a gross simplification of   complex factors that determine coronary blood flow.But it effectively clarifies a point ie  coronary blood flow is least dependent on coronary  stenosis (until  very late stages)

**Note further : This  hemodynamic  principle may not apply in acute occlusion as in STEMI  , where   acute  obstruction  often has a linear relationship with the quantum of blood flow.

By the way what happened to the above patient ?

Since he had significant angina there were no debates regarding management.  He  is posted for elective PCI this week-end .(We  can’t  get a stent just like that unless it is a real emergency  .Ours is a  Govt hospital !)

What is your take . Is it a going to be tough cross ?

I feel so , but my colleague Dr Gnanavelu   strongly  differs !

Let me post  our experience during PCI shortly.

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                                     Hypertension is considered a major cardiovascular risk factor.Hypertension  can have multiple physiological and pathological effects on heart . The common response to  raised arterial pressure is the hypertrophy of the left ventricle ( LVH). This can increase the risk of heart failure in few ( Mainly diastolic failure)  It is a leading cause for stroke  and   less often a  coronary event.

What links Hypertension and  coronary artery disease

                                           Coronary artery disease is almost synonymous with atherosclerosis. There is no separate entity called hypertensive coronary artery disease. But HT can accelerate the process of atherosclerosis. It is widely understood, hypertension can cause  physical endothelial damage and functional impairment of endothelial function.The physical damage ie enothelial disruption , or erosion is a very uncommon phenomenon . So currently  there is sufficient clinical experience  HT is considered dangerous for coronary artery only if it is with the  company of diabetes and hyperlipidemia. (This will seem controversial as it is against the findings of iconic Framingham trial!)

What the medical community refers to hypertension , may not be really so inside  for the coronary arteries.

                                             The relationship between brachial cuff blood pressure and the intra coronary pressure has very little linear relationship. So one should recognise it is the intra coronary hypertension that has a immediate impact on the coronary events. Now only , we are beginning to understand the complexities  of the relationship between HT and CAD. If we analyse a series of individuals HT per se is not a very serious risk factor for CAD* , but it is a number one risk factor for stroke. 

Why HT in isolation  often result in stroke , rather than a MI ?

While HT  is notoriously common to result  intracerebral hemorrhage, the same HT  would not cause  intramyocardial bleeds . Why ?

What is protecting the myocardium against this complication ?

                                      The exact mechanism  is not clear.Acute surges of blood pressure can increase the risk of stroke many times  but  rarely precipitate  a coronary event(  But may cause a LVF) . The reasons could be the coronary endothelial shearing stress is less than the cerebral blood vessels.Both cerebral and coronary circulation has  auto regulatory mechanism . The coronary auto regulation is more robust in that it does not allow  intra coronary pressures to reach critical levels .There is no clinically relevant intra myocardial hemorrhage reported  even during malignant hypertension.

*But a  high intra coronary pressure can sometimes  result in spontaneous coronary dissection and plaque fissure .Lipid mediated injury is vey much facilitated in a high pressure environment.

Has Controlling blood pressure  to optimal levels  , reduced the overall CAD morbidity and mortality ?

                    The answer is yes, ( But not an emphatic yes ! ) Some studies had been equivocal. It is very difficult to say , how much benefit is attributable to BP reduction  per se  and   how much is attributable to indirect effect on atherosclerosis prevention.

Hypertension during ACS

                            High blood pressure during an episode of unstable angina or STEMI can increase the myocardial oxygen demand and worsen the ischemia. It requires optimal control with nitroglycerine ( Preferably ) or beta blocker and ACE inhibitors.Even though HT is commonly associated  with ACS,  one can not be sure the ACS is preciptated by HT. Many times the sympathetic surge during an ACS keeps the blood pressure high.It is a common experience the blood pressure suddenly dropping to normal or hypotensive levels once the pain and anxiety is controlled.

Hypertension during thrombolysis

                           High blood pressure is a relative contraindication for thrombolysis.It need to be emphasised here, It is the  the fear of stroke that make  it contraindicated .The heart can tolerate  thrombolytic agents delivered at high BP .In fact logically ,  hemodynamically and also  practically it is obseved , thrombolytic agents administered at relatively high blood pressure (140-160 systolic) has better thrombolysis than a patient who is lysed at 100mmhg.

                       The coronary pressure head which contain the thrombolytic agent (streptokinase and others ) need to have pressure jet effect on the thrombus.So the  mean coronary perfusion pressure becomes  a critical determinant of success of thrombolysis.

                            It is a paradox of sorts , very high blood pressures are a relative contraindication for thrombolysis and at the same time normal pressure patients fare less well to thrombolysis.

 Final  message

                        Hypertension continues to be a major cardiovascular risk factor.It has direct and indirect effects on the heart.Generally HT is more of a risk factor for stroke than CAD.A slightly high BP ( Just around the  upper limits of normal or just above it ) has a hemodynamic advantage during thrombolysis.(Class C evidence )

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