July 19, 2008 by dr s venkatesan
CCU’S can also save patients with cardiogenic shock
Many of us would say ” never” or some may say “rarely” but in reality the answer is “yes it can ” slightly lower than Primary PCI . One could save atleast few lives every month by intensive medical management alone (Inotrope, vasodilator,pacing if needed ) in any coronary care unit.
So the message here is, not offering or doing a primary PCI in a patient with cardiogenic shock is not synonymous with inferior treatment or death. After all, in the much hyped SHOCK trial a significant no of patients survived in medical limb .
Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care | Tagged acs, cardiogenic shock, cardiology, drsvenkatesan, heart, myocardial infarction, stemi, ventricle | Leave a Comment »
July 19, 2008 by dr s venkatesan
Are we missing an entity called Primary cardiac neuralgia ?
Unexplained chestpain even after elaborate investigation is a very common clinical cardiac problem. Cardiac neural plexus has a complex network with mainly autonomic network ,with somatic projections. Neural dysfunction could occur in any organ which has rich neural network.Diabetes is the classical example of cardiac autonomic dysfunction and result in silent ischemia. The same disease can result in stimulation of type c nerve fibres that could result in cardiac neuralgic pain , which we may wrongly attribute to ischemia. One of the manifestation of this phenomenon occurs in syndrome X .
Future research is aimed at
Imaging cardiac neurons and sympathetic receptors will shed light on this . But clinical experience has taught us there should be many other sources of cardiac pain other than ischemia and neural pain definitely plays an important role.
It may take years to prove this by evidence !
Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs) | Tagged angina equivalent, atypical chest pain, cardiac neuralgia, cardiac plexus, chest pain, drsvenkatesa, neuralgia, post cabg, syndrome x | Leave a Comment »
July 19, 2008 by dr s venkatesan
Thousands of dissections happen in cath labs all over the world every day very rarely it is painful . The answer is not clear. Both have rich vasa nervorum. Aortic dissection involves media and smooth muscle . Coronary dissection may also be a equally painful , probably we are not recognising it ! or we attribute all chest pain in ACS to ischemia .
Deep dissections into the smooth muscle should be painful. Type c nerve fibers carry pain signals from heart
Answers welcome.
Posted in Cardiology -Interventional -PCI | Tagged acs, aorta, cardiology, cath lab, chest pain, coronary, dissection, drsvenkatesan, heart, madras medical college, nstemi, pci, stemi | 1 Comment »
July 19, 2008 by dr s venkatesan
Plaque fissure ,rupture and subsequent thrombois is the hallmark of acute coronary syndrome . Are these events painful ? We always attribute any chest pain in an ACS patient to ischemia of myocardium.Is that always true? Coronary artery also has a rich vasa nervorum that could be activated by plaque disruption.
Why we need an answer to this question ?
We are triaging patients for early invasive apporach based on chestpain .
Many patients may be subjected to revascularisation process for an non ischemic coronary pain !
Posted in cardiology- coronary care | Tagged acs, chest pain, coronary plaque, dissection, drsvenkatesan, interventional cardiology, nstemi, stemi | Leave a Comment »
July 15, 2008 by dr s venkatesan
Salvaging lung tissue is not the aim in pulmonary embolism , Hence Time window is a myth !
There is a time window for thrombolysis in myocardial infarction ( STEMI). This time window is to salvage myocardium before it dies.The average time window in STEMI is 12 hours. When does the lung start dying in Pulmonary embolism ?.Is salvaging lung tissue an aim in the management of pulmonary embolism ?. Not really .Lung parenchymal death occurs only in minority of patients with pulmonary embolism .
The bronchial artery continue to supply the lungs.
So the aim here is to restore pulmonary circulation and oxygenation. Hence there is no strict time window in the management of pulmonary embolism.
The General consensus is , one can attempt thrombolysis up to 7 days after diagnosing pulmonary embolism.
Beyond this time, it is believed thrombus gets organised and thrombolytic agents may be ineffective.
But this is only an assumption, in an individual patient thrombolysis may be done even beyond this period if warrented by clinical intuition .
Dr .S.Venkatesan .Madras medical college, Chennai.India .
Posted in cardiology -Therapeutics | Tagged acute pulmonary embolism, drsvenkatesan, pulmonary infarction, stemi, thrombolysis, time window | Leave a Comment »
July 15, 2008 by dr s venkatesan
Atrial septal defect is one of the common congenital heart disese. Surgical correction or device closure is indicated in all patients with significant shunts. Statistically for every ASD diagnosed with more than 2:1 shunt there must be is atleast three pateints with ASD with less than 2:1 shunt in general population. Do we diagnose it ? . Some may be miss diagnosed as PFO.
Posted in cardiology -congenital heart disease | Tagged asd, drsvenkatesan, left to right shunt | Leave a Comment »
July 2, 2008 by dr s venkatesan
Heart is a muscular pump .But it contains more of non muscular cells than contractile cells.
The average human heart which weighs 300 -400 grams . Contrary to the popular perception heart is not purely a muscular organ. In fact myocytes constitutes only 30% of heart mass. Rest formed by
1.Fibroblasts
2.Endothelial cells
3.Purkinje cells
4.Interstitial cells
5.Collagen
6.Fibrous skeleton
7.Extracellualr matrix.
Why is this important to recognise ?
Cardiac failure is not synonymous with myocardial failure .
Many times cardiac failure is due to supporting structure failure like in connective tissue disorders.
Exceesive fibroblast proliferation and resulting in fibrosis of heart.
Cardiac interstitial failure is new emerging clincal entity.
In future individual cell based therapy will aim at replacing specific cells that are defective or depleting.
Posted in cardiology-Anatomy | Tagged anatomy, cardiac failure, cardiology, collage, drsvenkatesan, fibroblasts, heart, LV mass, myocardium | Leave a Comment »
July 2, 2008 by dr s venkatesan
How is LAD angina differnt from RCA angina ?
Can we localise the “Angina related artery ” from the the type of chest pain ?
Patients with stable angia many times have multivessel CAD. There has been some correlation with radiation of anginal pain and the culprit artery.If the angina spreads to jaw or neck it is possibleit might indicate RCA(RIGHT coronary angina) but rarely it indicates LAD/LCX lesions. if the angina radiates to left shoulder it virtually ruels out a RCA disease
Source .Braunwald 1992 Edition
Dr.S.Venkatesan ., Madras medical college. Chennai.
Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), Tutorial in clinical cardiology | Tagged angina, angiogram, cardiology, coronary, drsvenkatesan, Heberdens, LAD, nstemi, RCA, STMI | 1 Comment »
July 2, 2008 by dr s venkatesan
Examinations in clinical cardiology
It is a brief early systolic outward thrust , followed by late systolic retraction felt by the palpating finger when the LV contracts and rotates , the LV apex and the adjacent interventricular septum hits against the chest wall. It is usually felt at the 5th left intercostal space just inside the mid clavicular line , lasting less than 30% of systole and occupying less than 3 square cms area.
Source : Horwitz ,signs and symptoms in clinical cardiology .1985. Lippincot
Should we always be able to palpate an apical impulse ?
Not really.If apical impulse is not felt in the sitting posture , one has to try in the left lateral position .In thick chest walled persons it may be impossible to feel the apical impulse in any postion. Many times it is so tiny it lies behind a rib and one will not feel it. In pericardial effusion also apical impulse is absent.
Posted in Tutorial in clinical cardiology | Tagged apical impulse, clinical cardiology, MD, palpation | Leave a Comment »
July 2, 2008 by dr s venkatesan
Aspirin confusion spreads to clopidogrel !
It all started with 75 mg clopidogrel in CURE study and others.
It went up to 150, 300, 600, and in some centres 900 mg.
No body knows how much clopidogrel optimally inhibits the platelet.
Aspirin had the same story three decades ago. It started from 40mg went up to 1200mg
and finally settled at 162mgs.
Why this confusion?
It is because there is no simple platletlet function tests available in bedside.
and also the wide safety margin of this drug.At what level clopidogrel is unsafe
is also not clear !
Answers are expected soon .
Posted in cardiology -Therapeutics | Tagged acs, aspirin, clopidogrel, nstemi, stemi | Leave a Comment »
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Dr.S.Venkatesan MD 