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What is the simple approach to bifurcation PCI ?

Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , on September 6, 2008| Leave a Comment »

There are numerous complex grading for bifurcation lesions available.

The one proposed by Medina is simple and most useful.

In this grading three segments

  • Proximal main vessel
  • Distal main vessel
  • Branch vessel

Are given a code 0, and 1 if  lesion is present or absent .

This grading gives simple and fast method to label a bifurcatiuon lesion and to asssess the response to PCI. The only issue here is the individual  lesions are not graded , for example branch vessel ostium just involved about 20 % is not addressed . Further TIMI flow in these vessels may also be incorporated

How medina grading can be used to assess effectiveness of

angioplasty  ?

A patient with 1.1.1  after the treatment should revert back to 0.0.0.  if converted into 0.0.(.5) may indicate a residual side branch lesion  .5 shall indicate 50% residual lesion, .3 , 30% etc

 

What is the best management strategy for bifurcation lesions?

The topic has been discussed extensively for over a decade in various forums.

Though the lesions and intervention techniques  appear complex the basic concept is simple.

Following is the 8 point algorithm

1. Assess the bifurcation lesion accurately.

2. Apply the general rule and ask the first question whether PCI is neccessary at all ? if decided for PCI

3. Stent the main vessel.Protect the side branch.  

4. Dilate the side branch with a balloon.(KIss or through the struts) 

5. Very rarely,  if the side vessel is more significant and large  stent it and balloon the main vessel.

6. Use drug eluting stents with caution .

7. Resist the temptation of using two stents unless the situation demands and is absolutely required.

8. Never attempt to do bifurcation angioplasty during ACS as apart of primary angioplasty.( Unless you’re extremely competent, even then aim of primary PCI is to salvage myocarium quickly , not to provide TIMI 3 flow in non IRA vessel.)

Dr.S.Venkatesan.Madras medical college.Chennai.

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Ironies in cardiology – Sinus rhythm loses the battle with atrial fibrillation in cardiac failure !

Posted in Uncategorized, tagged , , , , , , , , , , , , on August 26, 2008| 1 Comment »

 

The debate of rate control verses rhythm control in atrial fibrillation  goes on and on. The AFFIRM, RACE,PIAF, STAF the HOT CAFE all went against sinus rhythm in the last 10 years . This was one of the settled contoversies in cardiology . The conclusion was ventricular  rate control was no way inferior to rhythm control in patients with SHT, CAD population .This made the electrophyiologists wonder how can a natural rhythm fare bad ! . But the findings  were consistent .Rhythm control neither improved the quality of life nor  it reduced the incidence of stroke. The later finding was very surprising but the explanation was convincing as stroke in elderly was more related to SHT, CAD, DM etc than  AF itself. The source of emboli in ischemic stroke could come any where distal to LA .The big assumtion that all strokes in elderly  should come from LA appendage or the body  of LA was  premature and  wrong. What prevented stroke in AF was not restoration of SR but administration of oral anticoagulants with adequate INR.(2-3)

Having failed to document superiority in elderly  population   , the  logic machine  strongly suggested restoring SR  in patients with CHF,  will atleast provide hemodynamic and also survival  benefit .

And thus came the AF-CHF trial  published in NEJM 2008

Alas !  AF-CHF  also found there is no useful purpose of restoring sinus rhythm in patients  with atrial fibrillation and cardiac failure. In fact patients in SR fared little worse !

 Why . . .  why . . . why ?

Should we ask the seemingly absurd question !

Is sinus rhythm poorly tolerated by cardiac failure  patients ?

It is some times possible atrial fibrillation by itself could be a mechanism to amplify the  cardiac reserve by which it provides a  relatively high ventricular rate to improve the cardiac index  . Even though the optimal ventricular rate in AF is around 80-90 at times of need it has to increase to 120-130. Patients in class 3 CHF and AF often achieve this in times of demand .This is not possible in patients who are getting rhythm control drugs and further patients in SR can  not increase the HR suddenly from 80 -130  .

So is this a  wild imagination !   AF could be a safety valve mechanism in CHF to increase the HR . Where the atria come to the rescue of ventricle like a rate adaptive pacemaker .

The other logical* ! argument is that  there  is nothing wrong with restoring  SR , but the  methods to achieve and  maintain SR  is too cumbersome and results in adverse outcome .The currently available  drugs are too toxic for the purpose  .

If we have a simple and safe way to restore SR in these patients it should always be superior to AF .

But it is a well  known fact  that , whatever be the rhythm or rate the ultimate outcome will be dictated by the LV function, mitral valve function etc.

 Read abstract of AF-CHF

Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D., ., for the Atrial Fibrillation and Congestive Heart Failure Investigators

<!–

Rhythm Control versus Rate Control for Atrial Fibrillation and Heart Failure

— Denis Roy, M.D., Mario Talajic, M.D., Stanley Nattel, M.D.,  the Atrial Fibrillation and Congestive Heart Failure Investigators* –>ABSTRACT

Background It is common practice to restore and maintain sinus rhythm in patients with atrial fibrillation and heart failure. This approach is based in part on data indicating that atrial fibrillation is a predictor of death in patients with heart failure and suggesting that the suppression of atrial fibrillation may favorably affect the outcome. However, the benefits and risks of this approach have not been adequately studied. Methods We conducted a multicenter, randomized trial comparing the maintenance of sinus rhythm (rhythm control) with control of the ventricular rate (rate control) in patients with a left ventricular ejection fraction of 35% or less, symptoms of congestive heart failure, and a history of atrial fibrillation. The primary outcome was the time to death from cardiovascular causes.
Results A total of 1376 patients were enrolled (682 in the rhythm-control group and 694 in the rate-control group) and were followed for a mean of 37 months. Of these patients, 182 (27%) in the rhythm-control group died from cardiovascular causes, as compared with 175 (25%) in the rate-control group (hazard ratio in the rhythm-control group, 1.06; 95% confidence interval, 0.86 to 1.30; P=0.59 by the log-rank test). Secondary outcomes were similar in the two groups, including death from any cause (32% in the rhythm-control group and 33% in the rate-control group), stroke (3% and 4%, respectively), worsening heart failure (28% and 31%), and the composite of death from cardiovascular causes, stroke, or worsening heart failure (43% and 46%). There were also no significant differences favoring either strategy in any predefined subgroup.
Conclusions In patients with atrial fibrillation and congestive heart failure, a routine strategy of rhythm control does not reduce the rate of death from cardiovascular causes, as compared with a rate-control strategy.
 
 

 

 

 

 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

 

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What is pulse deficit ? What is the mechanism of pulse deficit ? Where does it occur ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , on August 13, 2008| 5 Comments »

Pulse deficit is a clinical sign wherein , one is able to find a difference in count between heart beat (Apical beat or Heart sounds ) and  peripheral pulse .This occurs even as the heart is  contracting , the pulse is not reaching the periphery.This can occur in few clinical situations .

1 . Atrial fibrillation.

2. Very early diastolic  ventricular  ectopic beats

3. Some patients with Pacemaker.

The mechanism is  , the ventricular contractions are  too weak and unable to open the aortic valve  (Or opens feebly*)  , but at the same time they are good enough to close the mitral valve. To open the aortic valve it has to generate atleast 60-80 mmhg pressure , while mitral valve closes even  as LV generates  8-14mmhg  .(LV/LA pressure cross over). So intermitently the  second heart sound  is missed while S1 is retained,  producing more heart sounds and less pulse count in the periphery. The S1 is either felt or heard at the apex but the corresponding pulse is missing . Further , this intermittent absence of  S2  results in totally irregular S1 /S 2 relation.

 

 

Why some of the contractions of LV is too weak to open the aortic valve ?

Because the RR interval varies , the ventricular filling also varies , diastole duration is constantly changing some of the diastole are too short  and LV hardly gets filled , as the LV force of contraction is directly decided by the LVEDV and LV  fibre length these contractions are too weak.

Other published studies

There has been some doppler observations ,where there is a midventricular LV blood flow reversal in atrial fibrillation that could  explain the pulse deficit . Mechanism of production of pulse deficit in atrial fibrillation: assessment by blood flow dynamics

Mawatari K, Sanada J, Kuroiwa N, Okumiya K, Nakamura K, Hashimoto S.

Second Department of Internal Medicine, Kagoshima University School of Medicine.

 http://www.ncbi.nlm.nih.gov/pubmed/3221309

What is the clinical significance of pulse deficit ?

Currently there is no great clinical significance of this phenomenon. But an astute clinician will pick up this sign and it may indicate underlying LV dysfunction. In patients with PPM,  pulse deficit  suggests  pacemaker malfunction .Some patients with cardiac tamponade &  pulsus paradoxus  systolic  blood pressure falls too low to make the pulse feeble or not palpable in the periphery .This situation may mimic a pulse deficit if not recognised.

Dr.S.Venkatesan ,Madras Medical College , Chennai, India

* What is the evidence for intermittent absence or feeble Aortic valve opening in Atrial fibrillation ? I could find this from the book written by Harvey Feigenbaum. whom we consider Father of Echocardiography

 

 

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Land mark studies in cardiology – Diastolic Heart failure : Ejection fraction is preserved all right , but “The life” is not !

Posted in Cardiology - Clinical, Cardiology -unresolved questions, Cardiology-Land mark studies, tagged , , , , , , , , , on August 11, 2008| 1 Comment »

The long standing controversy about diastolic heart failure is settled !

The perception that diastolic heart failure ( Now renamed as heart failure with preserved EF ) is less dangerous than systolic HF has been exposed by this land mark study by Owan TE, in 2006 (nejm) But unfortunately this information is not yet fully disseminated among the physician community. Hence this post, with due acknowledgment to NEJM & Owan et all.

Experts from the article

“The nosology of heart failure has been the
subject of much current debate, and some extreme
positions have been taken. The observation
that 22 to 29 percent of patients with diastolic
heart failure die within one year of hospital
discharge, and 65 percent die within five years,
is a reminder that we are facing a lethal condition,
regardless of its name. Owan et al. also
show that, in recent years, there has been little
improvement in survival rate among patients with
diastolic heart failure, in contrast to the improvement
in survival rate over time among patients
with systolic heart failure”

Have a look at the survival curve below, almost similar , surprise surprise ! DHF survival is not only worse ( in many ), than systolic CHF and further they respond poorly to treatment, compared to conventional systolic CHF .

Click below for the link to full text article

Short abstract :

Trends in prevalence and outcome of heart failure with preserved ejection fraction.

Owan TE, Hodge DO, Herges RM, Jacobsen SJ, Roger VL, Redfield MM.

Cardiorenal Research Laboratory, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

BACKGROUND: The prevalence of heart failure with preserved ejection fraction may be changing as a result of changes in population demographics and in the prevalence and treatment of risk factors for heart failure. Changes in the prevalence of heart failure with preserved ejection fraction may contribute to changes in the natural history of heart failure. We performed a study to define secular trends in the prevalence of heart failure with preserved ejection fraction among patients at a single institution over a 15-year period. METHODS: We studied all consecutive patients hospitalized with decompensated heart failure at Mayo Clinic Hospitals in Olmsted County, Minnesota, from 1987 through 2001. We classified patients as having either preserved or reduced ejection fraction. The patients were also classified as community patients (Olmsted County residents) or referral patients. Secular trends in the type of heart failure, associated cardiovascular disease, and survival were defined. RESULTS: A total of 6076 patients with heart failure were discharged over the 15-year period; data on ejection fraction were available for 4596 of these patients (76 percent). Of these, 53 percent had a reduced ejection fraction and 47 percent had a preserved ejection fraction. The proportion of patients with the diagnosis of heart failure with preserved ejection fraction increased over time and was significantly higher among community patients than among referral patients (55 percent vs. 45 percent). The prevalence rates of hypertension, atrial fibrillation, and diabetes among patients with heart failure increased significantly over time. Survival was slightly better among patients with preserved ejection fraction (adjusted hazard ratio for death, 0.96; P=0.01). Survival improved over time for those with reduced ejection fraction but not for those with preserved ejection fraction. CONCLUSIONS: The prevalence of heart failure with preserved ejection fraction increased over a 15-year period, while the rate of death from this disorder remained unchanged. These trends underscore the importance of this growing public health problem. Copyright 2006 Massachusetts Medical Society.

Other interesting article

Heart failure with preserved ejection fraction: dangerous, elusive, and difficult.

Eur Heart J. 2008 Feb;29(3):339-47. Nielsen OW, Køber L, Torp-Pedersen C.

BMJ editorail 2009

http://www.bmj.com/cgi/content/full/338/jan27_1/b52?ijkey=c7a29d35dc9d9dddf7d0e75c5b8d05014315c564

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Journal club debates : Can a “Aim of a study” be wrong ?

Posted in cardiology -Therapeutics, tagged , , , , , , , , , , , , , , , , , , on July 27, 2008| 2 Comments »

Peer review of an article even in major journals never scrutinise the “Aim of  a study ” . However big is the journal,  they seem to bother only about the authors, materials, methods, and statistical analysis.  If only they peer review an article , right from the “Aim of the study” like ,

  • Who asks the research questions?
  • Who  defines the aim of the study ?
  • Who decides which drug to be compared with which drug ?
  • Who steers the steering commitee of a trial ?

If only , we could answer these questions without bias , pharma industry and their  regulators  would have ,  far more better image than what they have now !

A typical example for , the aim of the study  to be  wrong  , is  the “ONTARGET’ study on telmisartan.

Here they ( Who ? ) raised an inappropriate  question of     “Non inferiority” of one drug with other  without any  valid reason to compare these two drugs that will benefit the man kind !

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Is there a time window for intervention in unstable angina /NSTEMI ?

Posted in Cardiology-Coronary artery disese, tagged , , , , , , , , , , , , , on June 26, 2008| Leave a Comment »

                                   ACS   is the  most common cardiac emergency .  Management of STEMI is relatively straight forward.  The  only decision that to be taken is the  modality of reperfusion. (Primary PCI   or thrombolysis.) There is no need to risk stratify  STEMI on arrival. All STEMI patients are considered high risk on admission. Whereas  NSTEMI consists of  a heterogeneous  population. They need to be   triaged into low intermediate  or high risk categorizes on arrival.There is two management  approaches for unstable angina .All high risk UA should enter early invasive strategy . And low risk and intermediate risk group will get early conservative management. 

                                       The principle of management of  UA differ from STEMI in a fundamental way , as there is no issue of myocardial salvage in UA .The primary aim is to provide relief from pain and prevent an MI. So in the strict sense there is no time window in unstable angina /NSTEMI.

 

                                       But it is generally considered 48 hours is the time limit for an early invasive approach.If the patient has crossed this time there is apparently no great difference in outcome for conservative and invasive approach. 

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