Feb
23

A Review Of Clinical Research In Ayurvedic Cardiology And The Way Forward

International Conference on Cardiovascular Research Convergence

A Review Of Clinical Research In Ayurvedic Cardiology And
The Way Forward

Sanjeev Rastogi

Clinical researches pertaining to Ayurvedic Cardiology refer to three different notions; they can be the researches based upon Ayurvedic fundamentals using Ayurvedic classical compounds, they can also be the biomedical researches based upon isolated herbs or their extracts or they can be the researches focusing upon lifestyle or dietary interventions endorsed in Ayurveda and aiming at reversal or prevention of the cardiac pathologies. Reviewing the clinical researches in Ayurveda is found intertwined with huge difficulties primarily because of unavailability of qualitative research works which are published and accessible. Ayurvedic researches in cardiology in India are largely marked with poor research designs and non publications which rendered to remain unavailable to most, working in similar fields.
Among published and accessible clinical researches also, there had been a huge variability among the
results even if the similar interventions and designs are used among similar disease population. For limited availability of RCT of Ayurvedic interventions in many cardiac conditions, a meta-analysis had not been possible in most of the cases. We also have observed that Ayurvedic interventions are not actually and fully tried in many prevailing cardiac conditions where Ayurveda may propose a dependable care . One such significant area could be the identification of suitable subpopulations based upon Ayurvedic prakriti analysis, where certain cardiac conditions may be more prevalent comparing to other groups. A simple cohort analysis of a disease population for their prakriti inclinations may give us an idea of prakriti subgroup more prone for a specific cardiac disease. A more specific and individualized preventive care may be proposed then after based upon preventive and promotive health care propositions of Ayurveda applicable to various dosha prakriti. We conclude that to utilize the potential of Ayurveda for conditions like prevention and management of cardiac conditions concrete efforts are needed to identify its actual resource followed by their scrutiny on various competitive research designs for exploration of their translational possibilities into clinical practice.

Feb
23

Can a Doctor Examine Forcibly A Patient Against His Wish If Brought By A Police Officer For Suspected Alcohol Intake?

Suppose in a road accident case, the police brings a person suspected of drunken driving for medical examination but he refuses the same.

The cardiologist should not do the exam without his consent forcefully.

This patient can only be seen only after he is arrested by the police and presented for MLR under section 53 CrPC, in which case reasonable force can also be applied.

 

Feb
23

Scope and Potential Of Cardiac Management In Ayurveda

International Conference on Cardiovascular Research Convergence

G G Gangadharan

Non-communicable diseases have taken precedence over the health needs of the society. Cardiovascular disease (CVD) especially ischemic heart disease is slated to occupy the top slot amongst the killer diseases worldwide by 2020 (WHO report on Global burden of disease, 2004). It is also seen that no single healthcare system has efficiently been able to address the issue of prevention and cure for diseases including CVDs. This also compels the need for evolving transdisciplinary therapeutic strategies to combat this killer disease.

Ayurveda literature has been the foremost to document the functioning of the hridaya (heart) much before the famed discovery of the circulation of blood by William Harvey in 1628. Much impetus has also been given to the mortality risks associated with any disease involving this organ and it has been identified as a Sadya pranahara marma. Though diverse treatments have been proposed to combat this disease, over time there has been a gradual decline in the clinical practice of cardiology using Ayurveda possibly due to a lack of exhaustive understanding of the pathophysiology of the disease. Cardiac diseases more often than not present with symptoms that necessitate life supporting care. The utility of aids like Electrocardiograms and radiological evidences for diagnosing the disease can also not be undermined to enhance the quality of care given to patients.

Though prima facie evidence for the management of acute cardiac conditions with only Ayurveda is lacking, there are ample clinical experiences wherein chronic/stable conditions can be co-managed with Ayurveda. The secondary offshoots arising out of a cardiac disease like edema, breathlessness, fatigue, fluctuating blood pressure, etc. can be contained to a large extent by judicious use of Ayurveda medications. A hlultipronged ‘Ubhayapratyanika chikitsa’ can be considered as the ideal approach to cardiac diseases. The treatment strategies must focus on Dosha shamana (alleviating the aggravated dosha) as well as Dhatu tarpana (enhancing the quality of the dhatu) and Ojo vardhana (enhancing the quality of the ojas). Rasayana drugs like Amalaki, Haritaki, Vibhitaki, Arjuna, Prashniparni, Pushkaramoola, Dadima, Pippali, Draksha, Shilajatu can effectively rejuvenate the cardiovascular system and enhance its effective functioning. In addition, Panchakarma procedures and instructions on Pathya sevana, appropriate to the patients’ physical condition should be integrated to optimize benefits.

The way forward for Ayurveda to achieve stronghold in managing cardiac conditions is to stringently document existing practices for such conditions and also to generate new evidence by using contemporary scientific methods.

Feb
23

Cardiac Transplantation: State Of The Art 2012

International Conference on Cardiovascular Research Convergence

Sudhir S. Kushwaha

Cardiac transplantation has come along way since the first human heart transplant in 1967. Based on historical data overall transplant survival is about 50% over 10 years. At the present time the main limitations to supply will include problems with the graft including rejection and allograft vasculopathy (CAV) as well as other comorbidities including infection, renal dysfunction and post-transplant lymphomatous disease. In order to control rejection we have to balance the risk of side effects, infections as well as the long-term risk of neoplasia. As far as immunosuppression is concerned in recent years there has been a decrease in the use of cyclosporine with an increase in the use of tacrolimus and some use of rapamycin.

By 10 years following cardiac transplantation over 50% of patients have evidence of CAV. This is a diffuse process, which affects the coronary arteries at all levels. Unfortunately the treatment options are somewhat limited and include the use of statins to control the lipids, treatment of CMV and the potential for PCI in limited cases. Rapamycin has been known to inhibit intimal hyperplasia and operates through the cell cycle. We have successfully used this agent to limit progression of renal disease as well as attenuate the development of CAV. This agent not only inhibits intimal progression but also decreases cardiac events.

One of the other observations we have made is that the extent of adverse remodeling and cardiac hypertrophy adversely influences outcome. The presence of concentric hypertrophy also been shown to decrease survival with increase in development of CAV.

One of the most interesting observations of the last decade is the discovery of chimerism of the transplanted heart. This was published in the New England Journal about decade ago. It therefore appears that stem cells may in fact have a role in the development of CAV. We have demonstrated that EPC colonies are reduced in CAV and this appears to have a correlation with coronary flow reserve. It therefore appears that Circulating progenitor cells from the recipient may playa role in populating the donor heart.
Understanding evolving field of stem cell biology may lead to the development all novel therapeutic strategies for prevention and treatment CAV

Feb
23

Chlamydia Pneumonia As An Infectious Agent To Induce Heart Disease

International Conference on Cardiovascular Research Convergence

Chlamydia Pneumonia As An Infectious Agent To Induce Heart Disease
Grant N. Pierce

Epidemiological findings have demonstrated an association of C. Pneumonia with coronary artery disease. LDL receptor deficient mice nasally infected with C. pneumonia will also generate plaque formation in an accelerated rate in comparison to controls. The atherogenic action of C. Pneumonia infection was only observed in a high cholesterol environment. The effects of C. Pneumonia on vascular thickening did not involve a host immune response but appeared to be induced by a direct effect on the vasculature. The molecular mechanisms responsible for this are not clear. However, C. Pneumonia
infection is associated with an increase in cell proliferation in the vasculature and this was closely associated with an increased expression of HSP60. The HSP60 expression directly induces cell proliferation. These atherogenic effects were accompanied by changes in vascular contractile function. Our data strongly support a role for infectious disease, and C. Pneumonia specifically, in atherogenic cardiovascular disease.

Supported by CIHR.

Feb
23

Last Patients on ICU Rounds Get Least Time

Padma Shri and Dr B C Roy National Awardee
Dr KK Aggarwal 

Doctors spent significantly less time with intensive care unit patients at the end of rounds as compared with the beginning.

The time decreased by about a minute per patient as clinical staff members made rounds in a 12-bed cardiothoracic intensive care unit (ICU).

Comparison of the first four and last four patients seen on rounds produced a statistically significant difference in the time spent with physicians and other participants in rounds, said Laura Jones, PhD, at the Society of Critical Care Medicine meeting.

To study time distribution during clinical rounds, Jones and colleagues accompanied clinical staff on 20 nonconsecutive weekdays during rounds in a cardiothoracic ICU. All patients had undergone coronary bypass surgery. On any given day, participants in rounds included one or more physicians, nurses, medical students, a pharmacist, a dietitian, and other healthcare providers. At the very least, an intensivist and one other physician participated in each session. The number of patient visits during the study period averaged 6.4, and rounds duration averaged 117.9 minutes. Interruptions accounted for about 10 minutes per rounds session and social interruptions for another 11.5 minutes.

Overall, the time spent with each patient during rounds decreased by 54 seconds per patient. Using a nine-patient session as an example, Jones said the clinical staff spent about eight minutes less with the last patient seen compared with the first. The difference between the first four and last four patients seen was statistically significant (P<0.05).

 


Feb
22

Mitogen-Activated Protein Kinases In The Regulation Of The Cardiac Fibroblast Cell Cycle

International Conference on Cardiovascular Research Convergence

Mitogen-Activated Protein Kinases In The Regulation Of The
Cardiac Fibroblast Cell Cycle

Cardiac fibroblasts, the most abundant cell type in the heart, are a major source of myocardial collagen, matrix metalloproteinases and several critical growth factors and cytokines. Unlike cardiac myocytes that are terminally differentiated and lose their replicative capacity after birth, cardiac fibroblasts retain their replicative potential throughout adult life. In response to myocardial injury, normally quiescent cardiac fibroblasts undergo phenotypic transformation into activated myofibroblasts that proliferate and produce matrix components to replace the damaged myocytes and facilitate healing. Over- expression of the fibroproliferative response, however, leads to cardiac fibrosis that can adversely impact myocardial remodeling associated with hypertension, myocardial infarction, and myocardial reperfusion injury. In this scenario, an important clinical goal would be the identification of cell cycle regulatory elements as potential therapeutic targets to regulate fibroblast hyperplasia and prevent excessive fibrous tissue formation in the diseased heart. Surprisingly, there is very little information on the mechanisms that regulate the cardiac fibroblast cell cycle. This presentation would discuss the distinct roles of p44/42 MAPK and p38 MAPK, and their downstream targets, in the regulation of G1-S transition in cardiac fibroblasts.

Feb
22

Role of Hydrogen Sulfide In Cardioprotection And Alteration Of Metabolic Syndrome In Experimental Animals

International Conference on Cardiovascular Research Convergence

Role of Hydrogen Sulfide In Cardioprotection And Alteration
O
f Metabolic Syndrome In Experimental Animals

Accumulating evidence has shown that hydrogen sulphide (H2S) acts as a novel gaseous signalling molecule which can freely diffuse across cell membranes in a receptor-independent manner and activates various intracellular targets. This distinct ability makes H2S an emerging pharmacological agent for the treatment of various cardiovascular diseases. Literature reports indicate that endogenously produced H2S involved in modulation of numerous biological events such as hypertension, cardiac injury, inflammation, and many others. H2S reduces arrhythmias and cardiac injury in hearts subjected to cardiac ischemia-reperfusion and improves myocyte survival, Cardioprotective effect of H2S is well known. However, cellular signalling cascades mediating these effects remained largely undefined. Recently, beneficial effect of H2S was linked with nitric oxide synthase (NOS) and cyclooxygenase-2 (COX-2) pathways. H2S also improves survival after cardiac arrest and cardiopulmonary resuscitation via NOS-dependent mechanism in mice. Our data also indicated that inhibition of NOS abrogates hydrogen sulfide-induced cardioprotection in mice. Similar to cardiac effect, H2S also play an important role in alteration of metabolic syndrome. Recently a decreased level of H2S has been reported in diabetic patients. Similarly, we also observed lower level of serum H2S level in fructose fed diabetic rats. Supplementation of raw garlic which provides H2S in in-vivo showed marked improvement of metabolic syndrome in type-2 diabetic rats. Our data indicated that H2S or its donors have beneficial effect against myocardial injury and metabolic syndrome. In future, development of new pharmacological agents modulating H2S level may open new avenues of therapeutic intervention against cardiac injury and metabolic svndrome.

 

Feb
22

New Anticoagulant Therapy For Patients With Atrial Fibrillation

International Conference on Cardiovascular Research Convergence

New Anticoagulant Therapy For Patients With Atrial Fibrillation

Atrial fibrillation (AF) is a common arrhythmia in elderly population and prevalence is increased with age. AF itself is not lethal, however, it is a risk factor for heart failure and thromboembolic stroke (5 – 6% in patients with AF). Both disorders may cause severe QoL impairment for which prophylactic interventions are necessary. In many cohort studies, the patients with AF have poor prognosis. The clinical studies including AFFIRM, J-RHYTHM which tested the outcome of the treatment; rate control vs rhythm control for AF, demonstrated that rhythm control is not better than rate control. In J-CHF
study which investigated the optional ~-blocker dose for treatment of CHF, it is demonstrated that heart rate reduction is more important than the dose of p-blocker. Thus, for prevention of CHF in patients with AF, rate control is a critically important approach for better outcome. Secondary, for the prevention of thromboembolic stroke, prophylactic treatment with anticoagulant is inevitable. For more than 50 years, vitamin K antagonist, warfarin has been used for this purpose. Warfarin, however, has a number of limitations including slow onset of action, a narrow therapeutic window, multiple drug and food interactions and the need for monitoring. Recently, new anticoagulants have been developed which inhibit thrombin or factor Xa. Several large clinical trials, RE-LY, ROCKET AF, and ARISTOTLE have been done and the results were published recently. ENGAGE AF- TIMI48 trial is now on going. A direct thrombin inhibitor, dabigatran and a direct Xa inhibitor, rivaroxaban have been approved for clinical use in many countries, and apixaban is now under review. These new anticoagulants will predominantly replace the warfarin for treatment of the patients with atrial fibrillation if they are indicated. Pharmacological characteristics and clinical benefits of these new drugs will be discussed.

 

 

Feb
22

Drug treatment of dyslipidaemia: What comes after statins?

International Conference on Cardiovascular Research Convergence

Drug treatment of dyslipidaemia: What comes after statins?

Amitabh Prakash

Lowering serum low density lipoprotein cholesterol (LDL-C) levels remains the most established method of preventing adverse cardiovascular (CV) outcomes in patients at risk. Hydroxymethyl coenzyme-A reductase inhibitors (statins) are currently the most effective drugs to lower serum LDL-C levels. However, at best they reduce serum LDL-C levels by 50% to 65% from pretreatment values and this may not be enough to attain goal serum LDL-C levels in all patients. The current goal serum LDL-C levels of <100 mg/dL (for patients deemed to be at high risk) and <70 mg/dL (for those deemed to be at very high risk) are achieved by only -50% and -15% of patients taking currently available drugs, respectively. Thus, there is an urgent need for drugs that lower serum LDL-C levels by mechanisms other than HMG-CoA reductase inhibition and can be used with statins, and for drugs that favourably alter the serum lipid profile by novel means. Drugs that primarily increase serum high density lipoprotein cholesterol (HDL-C) levels, e.g. niacin, or decrease triglyceride levels, e.g. fenofibrate, have failed to reduce the incidence of CV outcomes in clinical trials. New mechanisms to treat dyslipidaemia that are currently being actively
investigated include the following: phospholipase A2 (PLA2) inhibition (e.g. varespladib, darapladib, AMR1 01), microsomal triglyceride transfer protein (MTIP) inhibition (e.g. lomitapide), cholesteryl ester transfer protein (CETP) inhibition (e.g. anacetrapib, dalcetrapib), antisense RNA inhibition (e.g. mipomersen), apolipoprotein A 1 (ApoA 1) stimulation (e.g. RVX208), combined peroxisome proliferator- activated receptor (PPAR)-alpha and PPAR-gamma agonism (e.g. ZY H1), farnesoid X activated receptor antagonism (e.g. CDRI 80574) and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition (e.g. REGN727, ALN PCS, AMG 145). This presentation will summarise high-level results of late-stage clinical trials that are evaluating these agents. The clinical testing of these novel mechanisms, by pharmacologists and cardiologists, could dramatically change the future drug treatment of dyslipidaemia.

 

 

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