August 11, 2021 by admin0



Over the past several decades, cardiologists the world over, have tended to view coronary artery disease in terms of a “culprit lesion” hypothesis. This view allowed the materialistic school to focus on a specific lesion to develop site-specific diagnostic and therapeutic approaches.

First there was the quantification of a specific lesion using angiography, then Percutaneous transdermal coronary angioplasty (PTCA), intracoronary thrombolysis, atherectomy, stents and so on. They even transmitted this idea to their patients when reviewing their findings by using language like, “you had a blockage that we took care of.”

The impact and the persuasion is such that many patients come back and ask, “how is that lesion or blockage?” or “how do you know that it’s not come back?” and “should we take another angiogram to look at it?” They even indirectly imparted the idea that they took care of their entire problem when they treated that specific lesion.

Alternatively, when they could not find a specific lesion severe enough to account for clinical findings the tendency was to tell their patients that they only had a mild disease.

But it has become apparent even to the so-called modern school of therapeutics that if they are to make vital and lasting impacts on the outcome of this disease, then they must move beyond this type of narrow thinking. The culprit lesion notion was wishful thinking on their part that the key to this illness could be localized to a specific site in a portion of a large coronary artery. While this was important for the acute thrombotic occlusion found in the early hours of myocardial infarction, but the pathologists have become preoccupied with this finding.

How could the established and growing list of risk factor conditions for this disorder, which is all systemic such as increased LDL, hypertension, diabetes, inflammation, etc., resting on the fundamental bedrock of an active Tubercular (Psoro-sycotic or Psoro-syphilitic or Psoro-Syco-syphilitic) miasmatic state be expected to cause only a culprit lesion? or a singular pathology. Intracoronary ultrasound and even some angiography studies have identified more than one site of complex plaque or thrombus.

Multiple sites of rupture-vulnerable plaque are clearly present in those with what was previously termed only mild or minimal disease. And in those with more severe stenoses, it seems that the severe stenosis is a marker for many more rupture-vulnerable plaques at other sites.

Also, studies using radionuclide perfusion or directly measured coronary blood flow by Doppler wire have confirmed functional abnormalities at the small artery and arteriole level even when the more proximal lesions are not flow limiting.

These microvessels had generally been thought to be spared of atherosclerotic disease because of the absence of a large plaque. It is now clear that these dysfunctional microvessels fail to dilate appropriately to myocardial demands and contribute to malperfusion.

Thus, it seems reasonable to extend our thinking of this disease to one with generalized arterial involvement. Perhaps “panarterial” or even “arteriopathy” would be more useful terms to help better convey what we now know about the disease.

Furthermore, it is wise to know that the basic disorder is the “tendency to atherogenesis”, due to an activated tubercular miasmatic state, whereas arteriopathy is the pathological result of the disease. This notion conveys the message that the disease extends well beyond a localized site in a coronary artery. Indeed, early manifestations of panarterial atherogenesis are detected as endothelial dysfunction of the peripheral arteries of young individuals with risk factor conditions.


It is also likely that rupture-vulnerable plaque is present in other arteries but only becomes clinically apparent when rupture occurs in the coronary or cerebral arteries or the aorta. It has long been recognized that there is a heightened frequency of stroke associated with acute coronary syndromes.


The latter was believed due to cerebral embolization of ventricular mural thrombus. But it is likely that some of these strokes relate to embolization from complex lesions in the aorta, carotid, and vertebral systems. Further, the homeopathic remedies that help to decrease the adverse outcomes of this disease (including lifestyle modification) have their actions on at the luminal surface of all arteries (endothelium) through the vital force. Herein lies the most positive potential benefit from a shift in thinking toward a more systemic disease. If we were to make a concentrated attempt to think of this disease as a panarteriopathy rather than a culprit lesion, perhaps we could better influence patients and practitioners to heed advice relating to the need for constitutional treatments i.e to cure the tendency of atherogenesis.


As Late Dr. J.N.Kanjilal pens “theory, practice and experience are closely interlinked and mutually complementary. A theory, if it has to be substantial, must originate from practice, by the process of induction. A substantial theory usually evolves from the generalization of a particular fact observed in all cases of a particular branch of practice when it assumes the prestige of a Law of Nature. Thus a real theory originates from and is sustained by true practice.” In this way alone we may be better able to impact the outcome of this disease in the new millennium.

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