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In cardiac arterial interventional therapy, coronary angiograms provides key information to physicians for treatment strategy selection. However, it is hard to extract the information about arteries with CTO lesion in absence of contrast opacification and visualization of the CTO coronary arteries in angiograms. In this paper, we present an algorithm, which can predict the extension direction of artery with CTO and reconstruct the morphology of blocked artery in coronary angiograms. First, our algorithm segment the CTO artery angiogram and extract the artery skeleton. Second, an iterative approach is preformed to reconstruct the skeleton of blocked artery. Finally, our algorithm generates the simulated postoperative angiogram according to the skeleton image. The results demonstrate that automatic morphology reconstructing of CTO coronary artery with high accuracy and reliability is feasible.

It is a general believe that a blocked artery and its capillary are the main factor to determine myocardial infarction (MI) size and cardiac dysfunction. We have be plagued by the problem in repairing and regeneration of MI for many decades. How to improve the infarcted myocardium? By relieving the obstruction in coronary artery or promoting the angiogenesis of capillaries in the ischemic border zone? How to regrow the deteriorated capillary? From where? It is incredible to image the role of nearby non-ligated vessels in myocardial death and cardiac depression. In the present study, we show evidences that ischemic MI are not determined solely by the occluded artery, but also involved the nearby non-occluded artery, especially its capillaries that contributed nearly one-third effort to the MI. The mechanism is unclear yet, but this phenomenon is very interesting, offers a novel perspective to study heart failure. Arterial resistance to ischemia is a new object in heart failure research. It is unclear why some arterial vessel could survive in transmural MI, more interestingly it is unknown if capillaries could be regenerated from the residue arterial vessel in MI. The role of capillary both in ischemic artery and nearby non-ischemic branch in MI development is an amazing challenge. It is unknown why occlusion of left branch of LCA could degenerate capillaries on right branch of LCA. Inflammation probably plays a role in this phenomenon, but the knowledge of its mechanism is totally lacking even it indicates a potential path to new treatment strategy of ischemic heart disease.

Rapid, safe and effective arterial recanalisation to restore blood flow and improve functional outcome is the primary goal of hyperacute management of acute ischaemic stroke. This is possible either through thrombolysis or direct mechanical removal of clot from the blocked artery. Current evidence from randomised controlled trials shows that, for correctly selected patients, functional independence can be achieved in 32 - 71% of those who undergo clot removal. It is estimated that 10 - 15% of all ischaemic stroke patients have large-vessel occlusion and qualify for mechanical thrombectomy. It is important to have systems in place to identify and treat these patients.

Acute coronary occlusion, causing a heart attack, is best treated by prompt intervention and re-opening of the blocked artery. Such acute reperfusion, although saving many threatened heart cells from death, also paradoxically causes lethal reperfusion injury due to calcium overload in the mitochondria. There are protective molecular rescue paths that lessen the extent of such reperfusion injury. We discuss the evolution of these pathways during primitive times when heart attacks were rare. We believe that these paths evolved to counter acute stress situations in our ancestors when stimulated by intense physical effort, environmental conditions or hunting hazards, often accompanied by blood loss and hypotension. To test our hypothesis, we developed an underperfused model of acute heart failure with low perfusion pressure in the isolated rat heart to simulate the hypotensive response. We also increased the contents of free fatty acids (FFA) in the perfusate to supraphysiological levels to mimic the...

I began my career in 1994 as an interventional cardiologist, and I thought the world of medicine was totally mechanistic. My patient has a blocked artery; I have a stent and a statin in my toolbox; I fix the artery—end of story. There is nothing wrong with this approach in acute care. This type of medicine, the backbone of conventional medical education, can save lives. We were trained not to prevent disease but to treat acute problems. This training assumes patients are acutely ill and that the answer lies in some sort of “magic bullet.” They are not coming to us for preventive care.

Coronary artery disease (CAD) is the foremost cause of morbidity in the worlds industrialised nations. Consequently our ability in understanding the treatments available and the mechanisms of their success/failure is of particular importance as we strive to improve procedural success rates through the evolution of existing and the innovation of new interventional technologies. Today, the gold standard for treating CAD is to deploy a drug eluting stent (DES) in the blocked artery to first restore luminal blood flow and second to resist the body’s tendency to block the artery once more through its overly aggressive healing response known as restenosis. Intrinsically, the understanding of mass transport is elemental to all aspects of DES design from the type of drug used and the polymer release characteristics to the shape and thickness of the stent struts. Design optimisation of DES is vital to achieving increases in procedural success rates as the technology evolves, as is the case for its newest embodiment, the biodegradable DES. This chapter addresses issues fundamental to drug mass transport from DES, starting with an overview of CAD and associated interventional procedures. DES mass transport theory is then presented and followed by accounts of mass transport problem classifications employed by researchers under a number of deployment scenarios. The importance of experimental mass transport validation is highlighted and a computational investigation is developed to demonstrate how differences in DES deployment conditions alter drug concentrations in the artery wall.

Heart failure is a condition in which the heart muscle cannot function properly. It can result from the heart muscle becoming stiff over time or from a gradual weakening that results in a decreased ability to pump blood to the body. The weakening of the heart muscle, called systolic heart failure, is most commonly a result of processes such as heart attacks, heart valve abnormalities, uncontrolled hypertension, and viral illnesses, although a number of other conditions can cause the heart to weaken as well. Treating the underlying cause of the heart failure is the first step of management, whether it is through medicine or surgery to repair a blocked artery or a damaged heart valve or by controlling blood pressure. Even if the cause of the heart failure is unknown (idiopathic), the medical regimen used is the same as for the other causes of heart failure. A sensible diet with salt and fluid restriction, exercise, and medications such as angiotensin-converting enzyme (ACE) inhibitors and beta-blockers, often with diuretics (sometimes called water pills), are therapies aimed at relieving the stress the weakened heart is undergoing. In cases in which an individual is still suffering from the symptoms of heart failure (such as shortness of breath at rest or with minimal activity, fluid retention …

Stroke is a “brain attack” causing a blockage of blood to the brain that can lead to damage of the brain. It is like a blocked pipe under the sink that prevents water from going down the drain. A patient who has a stroke will typically develop weakness, numbness, or speech problems. (More information about stroke can be found on the next page.) Thrombolytic therapy is the injection of a medication—tissue plasminogen activator (tPA)—that breaks up a blood clot (“clot buster”). tPA can be injected with a needle into a vein (intravenous [IV]), an artery (intra-arterial [IA]), or both (IV/IA)—one after the other. It is like liquid “Draino” for the blocked sink (figure). Figure. Cartoon of a blocked artery in the brain that will cause a stroke if the blood clot that is blocking the blood to the brain is not removed/broken up. IV tPA travels in the blood throughout the body and can attack the blood clot. IA tPA is given through a catheter (straw) right where the clot is. IV tPA must be given very early after a stroke by a neurologist, emergency room physician, or other physician specifically trained in stroke. It is given within 3 hours after the first appearance of the stroke. IA tPA can be given up to 6 hours after the stroke has occurred under x-ray guidance to the blood vessels to the brain …

A consultant surgeon has won a challenge in the High Court to a “flawed” decision that his fitness to practise was impaired, in a case that raises several questions about the General Medical Council’s procedures. In 2007 a GMC panel imposed a 10 month suspension on Timothy Cheatle, a consultant general and vascular surgeon, over his treatment of an elderly patient, Mildred Swain, who had diabetes and vascular disease. He performed a femoropopliteal bypass graft at Oldchurch Hospital in Essex in April 2002 to bypass a blocked artery in her thigh. The graft became infected, and the joint between the graft and the artery leaked. By the time she was readmitted and taken to the operating theatre it was too late to save her. The panel found that Mr Cheatle failed to obtain and record informed consent, to take sufficient notice of signs of postoperative infection, and …

My first impression was of chaos as crowds of people milled around in a dimly lit corridor. This was the State Hospital in Skopje, the main healthcare facility in Macedonia, and I was accompanying my friend's mother to hospital on the day that she was due to be admitted for treatment to a blocked artery. My second impression was dismay. People shoved forward each time a door opened and a doctor appeared. There was no admissions desk or reception area, no organisation, seating, or even any signs. After pushing our way to the front we were sent to another floor where there was similar chaos. Eventually, the surgeon who had seen my friend's mother a month earlier called her into his small bare office and claimed that he had no record of her being due for admission that day. Tearful, she was sent home—a two and a half hour drive away—and told to call the …