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Posts Tagged ‘venkatesan sangareddi’
Posted in dr s venkatesan -Personal, general medicine, tagged best cardiologist india, cardiologist, cardiology fellows training, crash course on cardiology, dr s venkatesan, drsvenkatesan, ethical cardiologist, good cardiologist, madras medical college, teaching video in cardiology, venkatesan sangareddi on August 18, 2011| 10 Comments »
Posted in Cardiology -Interventional -PCI, My presentations, Uncategorized, tagged cardiological society of india, csi kolkatta, department of cardiology cardiommc.org, dr s venkatesan, g gnanvelu, madras medical college chennai, primary pci, primary ptca, spontaneous thromolysis, venkatesan sangareddi, www.cardiommc.org, www.drsvenkatesan.com on December 8, 2010| Leave a Comment »
It is well recognised for STEMI to get aborted spontaneously or through intervention.
Can a glamorous procedure like Primary PCI be redundant ?
Yes of course . This paper, is about how a planned Primary PCI can go awry . . . Presented in the Annual scientific sessions of cardiological society of India Kolkatta December 2010.
Summary of the presentation
ABORTED AND ABANDONED PRIMARY PCI
S.Venkatesan G.Gnanavelu.R.Subramanian .Geetha Subramaninan
Madras Medical College. Chennai
Primary PCI has become the standard of care for acute STEMI in all those eligible patients. Apart from the individual & institutional expertise ,the key to success lies in expediting the symptom to balloon time to less than an hour.
Even though STEMI is characterized by acute total obstruction , it is also a fact during this critical time window , a less recognised positive phenomenon takes place within the ill fated coronary artery. Intrinsic fibrinolytic activity gets activiated and begins to take on the thrombus head on .It should be recalled this is the earliest intervention in STEMI by natural forces , with zero time window . The power of this natural lytic process has never been easy to predict and quantiate . But we have often realised such a phenomenon do occur often and is referred by various terminologies like spontaneuous thrombolyis, aboted MI etc .The exact incidence is not estimated .In this era of primary PCI we have found a new opportunity to confirm this concept.
It has been observed during primary PCI , an occasional patient may have either a totally patent IRA or a minimal & insignificant lesion like luminal irregularity .This has subsequently led on to cancellation of the procedure .We report our experience with two patients with this particular situation .One patient with IWMI with a time window of 6hours had a totally patent RCA. Even , the luminal irregularities were difficult to locate .The other patient had anterior MI with ongoing ischemic pain.He was taken up for primary PCI.The initial angiogram showed a total mid LAD obstruction . As soon as the guidewire reached the thrombotic lesion the artery opened up wth a TIMI 3 flow .There was no residual lesion or thrombus noted. Both of the above patients were young , smokers . 2b 3a antagonists were not administered. We infered, both had thrombotic STEMI and presumed to had either spontaneous reperfusion , or reperfusion assisted by dye injection & guidewire manipulation. They were shifted out of cath lab with a new code of aborted primary PCI and were discharged with normal LV function .It need to be realised here, a distinction must me made between aborted PCI and abandoned or failed primary PCI as the later connote a negative outcome. The causes for abandoning primary PCI are due to complex lesions like bifurcation /Trifurcation lesions , triple vessel disease with difficulty in identifying culprit lesions.A Primary PCI is considered failed when the IRA patency is not accomplished or failure to sustain myocardial flow inspite of IRA patency (No-Reflow) . These patients may end up in CABG or occasionally fall back on thrombolysis which was considered a inferior modality just few hours earlier !
. We conclude , in the management of STEMI , primary PCI once contemplated need not always reach it’s logical conclusion. There are situations it can get aborted or abandoned at various levels . Aborted primary PCI due to spontaneous lysis though uncommon , can be a therapeutically and financially rewarding concept for the patient and physician .
Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged auscultation, bmj, clinical cardiology, drsvenkatesan, epicardium, lancet, parietal pericardium, pericardial effusion, pericardial rub, pericarditis, spodick, to and fro murmur, venkatesan sangareddi, visceral pericardium on September 28, 2008| 6 Comments »
Heart is externally covered by two layers of pericardium . Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces come into contact , pathological rub takes place.It is heard whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon clinical sign .
Common clinical conditions
- Acute pericarditis
- Uremic pericarditis.
- Rheumatic pericarditis
- Post myocardial infarction
Pericardium has two layers .
There are four possibilities for pericardial rub to take place.
The rub can occur
1.Between the two layers of pericardium
2.Between the visceral pericardium and the epicardial layer of heart*.
3.Between parietal pericardium and the chest wall
4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )
The second and third mechanisms are very rare.
We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of diaphragm especially the contagious ones from abdomen , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.
*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?
Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and are located sub epicardially.
How many components of pericardial rub are clincally heard ?
Pericardial rub classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.
Superficial , scratchy, high pitched ( Can also be low pitched)
Left sternal border , left 2nd or 3rd space .Best heard in sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.
What is the mechanism of pericardial rub in the immediate post MI phase ?
Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture and hemorrhagic effusion if anticoagulants are used.
What is the relationship between pericardial effusion and pericardial rub ?
Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.
Rubs after contusion chest and fracture ribs can be with the chest wall and may have no relationship with effusion.
Is pericardial rub a painful condition ?
Pericardial rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.
What is pleuro pericardial rub ?
This clinical entity is poorly defined , often taught by veteran professors in clinical auscultation classes.It can be heard in the mid segment or diaphragmatic pleuritis with or without pericardial effusion in patients with atypical pneumonias.