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Posts Tagged ‘intra coronary hypertension’

Coronary bloodflow is primarily known, to occcur as a diastolic circulation. Does that in any way mean coronary artery diastolic pressure, can exceed the systolic pressure ?

A. No. diastolic BP can never exceed systolic BP in side the coronary artery.

B. Yes. Coronary diastolic BP is higher than systolic, since there is little blood flow during systole due to myocardial compression.

C. There is not much difference between systolic and diastolic pressures, within the coronary artery . We need to bother only about mean perfusion pressure.

D.It is true, the coronary blood flow is compromised in systole and primarily occur in diastole .Still, the epicardial coronary arterial compresssion is not that significant. Hence systolic pressure blunting is negligible. This is called the pressure -flow paradox.

Answer : D (Ref Image 2)

What is the normal intra-coronary arterial pressure in systole and diastole? I could not get a clear answer to this question. Logically it should be sane as in radialartery 120/80mmhg. Surprisingly, most literature discusses only coronary blood flow, which primarily takes place in diastole. (Does that mean the pressure would be less in diastole, so that blood flows easily?) The complexity in understanding intra-coronary pressure , is because, we don’t know the exact blood volume, flow vs pressure relation in this dynamic organ.Further, mechanical force/pressure exerted by the muscle ,can it be recorded , within the lumen , and quntify it sepearately ?

The classical illustrations that are found in cardiac physiology literature about the dominance of coronary blood flow during diastole (Image source Ref 2)

During FFR studies the Intracoronary presssure curves almost mimic radial pulse. No where we could see the effect of mechanical compression . It is likely , the epicardial coronary artery do not get compressed that much , only the micro circulation gets squeezed.

Image 2: source Yuhei Kobayashi et al JACC 2017

We realise ,coronary perfusion pressure, mean coronary arterial pressure, and coronary arterial wedge pressure are more important than systolic and diastolic pressures . The mean coronary artery pressure is around 45 to 60 mmHg backed up with good autoregulatory mechanism. We are not clear how this autoregulation is modified by lesion tightness. Documentation of true coronary arterial systolic BP in physiology and various pathologies is an important academic vacuum that youngsters can explore.

1.Clinical Implication : Does LV dysfunction has a favorable efffect on coronary perfusion ?

If LV contraction interferes with coronary blood flow, patients with severe LV dysfunction, may gain some advantage as systolic blood flow can happen more easily, and myocardium is perfused better, provided the aortic systolic pressure not too low enough.

2.How common is angina in DCM ? and Why ?

Angina in DCM is an exception despite elevated LVEDP. Is the above logic explain why very few dilated cardiomyopathy patients experience angina? Even in ischemic cardiomyopathy, once it sets in, Intensity of angina is mitigated or completley eliminated.(of course at the cost of failure). Is it nature’s response to prevent angina?

3.Why systemic hypertension is a weak coronary risk factor ?

Unlike the brain, where stroke risk is directly related to systolic BP, fortunately sudden systolic spikes rarely get a chance to attack the coronary endothelium as much of the coronary lumen is relatively closed (? to be confirmed , atleast during rapid ejection phase of systole) In this context, we can also be happy there is no risk of myocardial hemorrhage due to HT. However, there is evidence that diastolic BP carries much risk for CAD, as do Isometric exercises when DBP exceeds out of proportion to systolic BP.

4.Differential intra coronary pressure , RCA VS LCA is well knwon asthe RV contraction is not good enough to compress the RCA.This adds a new hemodynamic concepts in RCA CAD.(We have done a study where we found thrombolysis was more effective in RCA apparently due to bi-modal continuous delivery of the lytic drugs, unlike the left system)

5.During CPR , what would be coronary hemodynamics of chest compression ?

When we compress, it is systemic systole, and when we release it becomes coronary diastole. In fact there is now evidence to suggest , too rapid and hurried contractions reduce the success rate of CPR. The inter compression time is to be atleast 4 or even 5 full seconds, to enable coronary perfusion.The mean pressure during CPR is to be atleast 40mmhg. (Yannopoulos D et al , Resuscitation. 2005)

Final message

It is surprising why we are not recording intra-coronary pressure directly and trying to understand this. We need to go 100 years back for that Wiggers article in search of truth. (Ref 1). This is an area of good research for cardiology fellows. Also, next time,when you do FFR or IFR, ask this question : Why proximal reference pressure is taken at the aortic root instead of just before the lesion ?

Reference

1.Harold D. Green, Donald D. Gregg, andCarl J. Wiggers 31 July 1935

2.https://derangedphysiology.com/main/cicm-primary-exam/cardiovascular-system/Chapter-476/coronary-blood-flow

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                    circulatory                                                                            A normally  functioning  circulatory system is vital for our survival . We have about 6000 ml of  blood, circulating  all over the  body in an  approximate time of 15-20 seconds.The pressure at which this blood moves across the body is called the blood pressure . Hypertension  or simply , high blood pressure is an undesirable  hemodynamic disturbance  in human circulatory system.Systemic hypertension is the most common type of hypertension. The blood pressure is primarily  dependent  on the status of the blood vessel(vascular resistance)  and cardiac contractility. This regulation is under  many neural and hormonal factors.Further  the blood pressure varies depending  upon the blood vessel calibre, and the local milieu.There is a progressive drop in blood pressure from major arteries to the small arteries .The pressure drop is maximum  across the arterioles to reach the venules .The venous circulation has the lowest pressure, it ends up at right atrium with a mean pressure of 0- 5mmhg.

Importance of regional variation of blood pressure.

It should be realised  ,  each organ has it’s own regulated blood pressure.The brain  perfuses by the  intracerebral pressure .The lungs decide how much should be the pulmonary arterial pressure.The kidney not only controls it’s own pressure but also  has a major regulatory role in  systemic pressure by rennin angiotensin system.The examples are numerous, portal system has it’s unique pressure controlling hepatic hemodynamics. The  retinal blood vessels regulate  intra ocular pressure. While the human  circulatory system has a wide variation of blood pressure  across the breadth and length of vascular system,  it is ironical a single snap shot BP with a brachial cuff is used  to define the normality and if it is normal every thing is thought to be  hunky dory !

 

 

It is widely acknowledged now , aging of humanity  is nothing but aging of our vascular system

                                    So we should have new parameters to assess individual organ’s vascular health as well as the currently popular systemic vascular health.The single important factor that determine coronary endothelial damage is the intra coronary pressure.It is never taken into account in any of the cardivascular mortality studies. This is the prime reason for  the widely prevalent conflict in the cardiology literature , namely : Controlling systemic  blood pressure has poor correlation with  cardiovascular outcome. Many of the so called normotensive individuals  have serious hemodynamic injury in their  coronary arteries.This was made apparent in the  ASCOT LLA  study , in which patients with  near normal blood pressure also benefited from statin therapy , implying  endothelial damage could occur at any level of systemic blood pressure.

What is the normal intracoronary pressure  ? When do you diagnose intracoonary hypertension?

The normal intracoronary pressure is around 40mmhg . Intra coronary hypertension as a clinical entity  is yet to be  recognised . There is no defintion available for intracoronary HT  , intracerebral hypertension as well. 

It’s still a  long way to  go , for the cardiology and neurology  community to assess non invasively  intracoronary pressures and  intra cerebral arterial pressure to prevent  coronary events ant strokes.

Final message

Simple risk prediction using brachial cuff blood pressure is a grossly unscientific method (Sorry, i really mean it ) to assess one’s vascular health.There has been  few attempts like vascular endothelial health assessment by fore arm blood  flow , central aortic pressure (Instead of brachial cuff pressure) as an  index for risk predictment and  assessment for hypertension is suggested.

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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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