Pathophysiology of Spontaneous Coronary Artery Dissection Determines Anticoagulation Strategy.

Spontaneous coronary dissection is an uncommon disorder, lacking convincing pathophysiologic evidence. Scientific statements and state-of-the-art articles suggest intramural hematoma from bleeding vasa vasorum is the cause. Evidence is based on limited invasive evaluation with optical coherence tomography. This assumption, therefore, suggests anti-coagulation be discontinued. Mechanical shear forces, intraluminal pressures do not support bleeding vasa vasorum closing a higher luminal pressure vessel. The endothelium's role in inflammation, thrombosis, and repair suggests the pathophysiology is failure to repair endothelium with the lack of repair as the nidus of disruption. A tear ensues and can spontaneously reseal. The lack of inflammatory cells in pathological specimens and association with another poorly understood disease fibromuscular dysplasia supports the etiology of both entities as failure to replace endothelium. The endothelium is the fulcrum of both inflammation and thrombosis. The ability to heal the rift supports conservative therapy. Anticoagulants and antiplatelet reduce thrombosis and inflammation which will ensue when the endothelium is disrupted. These agents will substitute for the failed endothelium allowing thrombosis to be kept in check, reduce inflammation, and promote healing. This thesis and the state-of-the-art articles do not present clinical outcome data. Both support conservative interventions. Anticoagulation recommendations are however in opposite realms. Failure to repair endothelium suggest additional therapies of statins, exercise, smoking cessation will increase circulating stem cells may reduce future events and slow the progression of fibromuscular dysplasia. Future directions in understanding this disease and new therapies requires measurement of repair mechanisms such as the quantity of circulating endothelial progenitor cells.

Cost to Save a Life in Heart Failure: Health Disparity Costs Lives.

Objective The purpose of this paper is to assign a dollar value to life-saving medication, surgical procedures, and medical devices. The knowledge of the wide variation in the cost of drugs, surgery, and devices allows providers and patients to choose higher-valued therapies. Cost is a significant barrier to health. The current reimbursement system is complicated, representing a significant barrier to saving lives by promoting health disparity. Background The cost analysis of heart failure therapies is an important tool in the education of physicians, patients, and vendors of the intervention. The analysis demonstrates disparities between heart failure therapies. The cost to save a single life is calculated from annualized absolute mortality risk reduction, trial length, and estimated 10-year costs. The method allows comparisons of drugs, devices, and surgery. Methods The 10-year cost of drugs is 120 months times the cost of a drug/month as listed by the website GoodRX.com. The 10-year cost of surgery or device therapy was determined from a cost analysis found by a Google search of the literature. When wide ranges were reported, the mean value was selected. 1/absolute mortality risk reduction X 100 is the number needed to treat to save a life annualized for the mean length of the study. The cost to save a life can then be computed by the following formula: Cost/life saved = (10-year cost/annualized absolute mortality risk reduction) X (100) Results Beta-blockers and spironolactone had the lowest cost per life saved at $13,333 and $21,818, respectively. Defibrillators are the most expensive at $6,417,856. Valsartan/sacubitril has a cost of $1,127,733. Dapagliflozin, the newest class of heart failure drug, costs $4,853,200.  Conclusions Calculating the cost to save a life gives insight into the value of therapies and demonstrates disparities. It is a means of comparing drugs and devices. New drug therapies are costly, not affordable, and serve as a barrier to the successful treatment of heart failure.

Why We Fail at Heart Failure: Lymphatic Insufficiency Is Disregarded.

Is the definition of heart failure too narrow, not allowing research into compensatory mechanisms, comorbidities, right heart function, and lymphatic function? A review of the absolute mortality of heart failure drugs and devices suggests a modest improvement in outcomes. Absolute mortality from common comorbidities, including renal insufficiency, arrhythmia, conduction deficits, pulmonary hypertension, anemia, obstructive sleep apnea, infection, inflammation, edema, ischemic heart disease, and diabetes II, is significant. The lymphatic function is involved in short, intermediate, and long-term compensation for a failing heart and plays a role in most of the comorbidities. A better definition of heart failure is: Heart failure is a complex clinical syndrome that results from any structural or functional impairment of right or left ventricular filling or ejection of blood and failure of peripheral compensatory mechanisms. Lymphatic function from the anatomic, fluid management, immune modification standpoints requires study. New therapies from this analysis will improve patients with congestive heart failure.

Pathophysiology of narrow complex dilated cardiomyopathy insight derived from the velocity equation: velocity = distance/time.

The pathophysiology of narrow complex dilated cardiomyopathy is not defined, so therapeutic options are limited. By utilising the velocity equation, the pathophysiology of narrow complex cardiomyopathy allows above normal conduction propagation velocities. There are two pathophysiological theories that allow above normal conduction velocities and failure to capture the myocardium: (1)insulating fibres of the conduction system extending beyond the apex and (2) reduction of axon branching. A patient with narrow complex cardiomyopathy was subjected to graded increase in amplitude and pulse width pacing to overcome the failure of native conduction to capture the myocardium. Peak systolic strain maps demonstrated a progressive increase in apical contractility with increasing pulse width and amplitude. Ejection fraction improved from 17% to 31%. Understanding the pathophysiology of narrow complex cardiomyopathy leads to proposed therapies. One potential pacing therapy is multi-lead pacing at high amplitude and pulse width to capture myocardial cells not captured by native conduction.

"Observational Medicine" should be replaced by "Real Science".

Science is defined by fundamental principles that can be modeled to explain observations and predict new findings. Clinical trials have not achieved this status. The trials generate new observations and lack the ability to predict future outcomes. The following hypotheses are generated: 1. Biology has no defined fundamental principles that can be modeled to explain observations and predict new findings. 2. Observational Medicine has advanced our knowledge but has not elicited fundamental principles that could predict future outcomes in individual patients. 3. A biologic model of regeneration/degeneration moderated by inflammation framed by 6 laws of biology can make predictions. 4. Biology can be quantified. Observational Medicine from Hippocrates, through Framingham and the Women's Health Initiative are examined. These trials have advanced our knowledge but have not elicited fundamental principles that could predict future outcomes. A set of fundamental principles of biology and a model based on regeneration/degeneration modified by inflammation has been previously reported. These laws represent empirical facts and no exceptions to these laws have been realized. The model suggests the observations from Framingham could be explained by the quantity of circulating stem cells and the inflammatory status of the patient. Clinical trials that select patients by their quantity of stem cells and inflammatory status would be more efficient than selection by risk factors. This same model can explain the inability of the Women's Health Initiative to determine the female advantage over men in coronary heart disease. This model is exploited to make predictions in coronary disease, heart failure, and is used to explain disease processes, paradoxes and make predictions. Mechanical statistical entropy is method that can quantify biologic processes.

Applying laws of biology to diabetes with emphasis on metabolic syndrome.

The listed laws of biology will be applied to diabetes mellitus and metabolic syndrome. (1) Biology must be consistent with the fundamental laws of physics and chemistry. (2) Life, as opposed to non-living, exhibits negative entropy (known as syntropy), capable of creating order out of chaos. (The energy to support negative entropy is yet to be defined.) (3) The cell is the fundamental unit of biology. (4) The cell must be in homeostasis with its environment. (This property enables the process of evolution. In other words, the environment changes life.) (5) There must be a distinction between self and the environment. (Immunity and inflammation are the defenses against invaders from the environment and responsible for repair of damaged and senile cells.) (6) Electromagnetic information transfer is necessary for development and regeneration. (Life and, more specifically, regeneration of tissue will not exist in a non-electromagnetic environment, denervation results in atrophy.) A new model of disease derived from these laws is that health exists when degeneration and regeneration are in balance. Inflammation is the fulcrum between the two, being both beneficial in repair and detrimental by promoting degeneration. This model leads to a number of hypotheses.

Should we establish a new protocol for the treatment of peripartum myocardial infarction?

Peripartum myocardial infarction is a rare event that is associated with high mortality rates. The differential diagnosis includes coronary artery dissection, coronary artery thrombosis, vascular spasm, and stenosis. Our evaluation of 2 cases over a 5-year time period has led to a hypothesis that peripartum myocardial infarction is an immune-mediated event secondary to coronary endothelial sensitization by fetal antigen. In our patients, we supplemented standard medical therapy with immunotherapy consisting of corticosteroids, plasmapheresis, and intravenous immunoglobulin. Herein, we present our most recent case-that of a 29-year-old black woman (gravida V, para IV), 2 weeks postpartum with no relevant medical history. She presented with a 1-week history of chest pain. Initial electrocardiographic and cardiac biomarkers were consistent with acute coronary syndrome. Echocardiography revealed reduced systolic function with inferior-wall hypokinesis. Angiography revealed diffuse disease with occlusion of the left anterior descending coronary artery not amenable to revascularization. We were successful in treating the myocardial infarction without the use of catheter-based interventions, by modifying the immunologic abnormalities. Two cases do not make a protocol. Yet we believe that this case and our earlier case lend credence to the hypothesis that peripartum myocardial infarction arises from sensitization by fetal antigens. This concept and the immune-modifying treatment protocol that we propose might also assist in understanding and treating other inflammatory-disease states such as peripartum cardiomyopathy and standard acute myocardial infarction. All of this warrants further investigation.

Mycotic pseudoaneurysm of the aortic arch with purulent pericardial effusion.

A 67-year-old woman presented with dyspnea on exertion and a diminished left radial pulse in comparison with the right. She had signs and symptoms of cardiac tamponade. A computed tomographic (CT) angiogram of the chest revealed an aortic arch pseudoaneurysm along the lesser curvature and a large pericardial effusion with the density of blood. Upon pericardiotomy, a nonhemorrhagic thick purulent effusion (Streptococcus milleri) was discovered in the pericardial space. Replacement of the aortic arch was performed with a rifampin-soaked Dacron tube graft, with the patient under hypothermic circulatory arrest.

Enhanced external counterpulsation is a regenerative therapy.

Enhanced external counterpulsation (EECP) is used for the treatment of severe angina and heart failure in patients who are not candidates for revascularization. The clinical benefits of EECP extend well beyond the time period of any hemodynamic effects, but the cause of this prolonged effect is not understood. The prolonged clinical benefits suggest EECP could be a regenerative therapy. This study was performed to determine whether EECP increased circulating hematopoietic progenitor cells (HPCs) or endothelial progenitor cells (EPCs) and thus be a possible regenerative therapy. The proposed mechanism of the increase in regenerative circulating stem cells is the enhanced shear forces induced on the endothelial boundary by the flow reversal produced by the sequential inflation of the pneumatic cuffs during EECP therapy.

Accuracy of accelerated cine MR imaging at 3 Tesla in longitudinal follow-up of cardiac function.

The ability of fast, parallel-imaging-based cine magnetic resonance (MR) to monitor global cardiac function in longitudinal exams at 3 Tesla was evaluated. Seventeen patients with chronic cardiac disease underwent serial cine MR imaging exams (n=3) at 3 Tesla. Data were acquired in short-axis orientation using cine steady-state free precession (SSFP) with a spatial resolution of 2.5 x 1.9 mm(2) at 45 ms temporal resolution. Multislice imaging (three slices/breath-hold) was performed using TSENSE acceleration (R=3) and standard single-slice cine (non-TSENSE) was performed at identical locations in consecutive breath-holds. End-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction (EF) and myocardial mass (MM) of both cine approaches were compared for individual time-points as well as for longitudinal comparison. TSENSE-cine did not show significant differences for EDV (2.6 ml; P=0.79), ESV (2.2 ml; P=0.81), EF (-0.3%; P=0.95) and MM (2.4 g; P=0.72) in comparison with non-TSENSE. Longitudinal ANOVA analysis did not reveal significant differences for any parameter, neither for non-TSENSE data (all P>0.7) nor for TSENSE data (all P>0.9). Multifactorial ANOVA showed non-significant differences (all P>0.7) at comparable data variances. Data acquisition was significantly shortened using TSENSE. Threefold accelerated multislice cine at 3 Tesla allows accurate assessment of volumetric LV data and accurate longitudinal monitoring of global LV function at a substantially shorter overall examination time.

Relation of atmospheric pressure changes and the occurrences of acute myocardial infarction and stroke.

Previous studies have demonstrated variation in vascular events with respect to season and time of day. Changes in barometric pressure display daily and seasonal variations and could modulate the occurrence of vascular events. The objective of this study was to determine whether a relation exists between changes in barometric pressure and occurrence of stroke or acute myocardial infarction (AMI). A retrospective analysis of hospital admissions for AMI and stroke from 1993 to 1996 in central Texas was related to changes in atmospheric pressure that were obtained from the National Climatic Data Center. Patients who had AMI (n = 1,327) or stroke (n = 839) were identified from a computerized hospital database. Mean atmospheric pressure, greatest change in pressure, and rate of change in pressure per 24-hour period were computed. One-, 2-, and 3-day and seasonal groupings of cardiovascular events were related to corresponding changes in barometric pressure. The fall and winter seasons had the highest variability in atmospheric pressure readings. There was a significant correlation (p = 0.0083) between a decrease in atmospheric pressure and the occurrence of AMI the day after a pressure decrease, especially during the fall and winter seasons. No relation between stroke and atmospheric pressure was demonstrated. In conclusion, we conclude that rapid decreases in barometric pressure are associated with the occurrence of AMI but not of stroke.

Return to work and the person with heart failure.

Heart failure (HF) is an economic and social problem for millions of Americans. Medical bills and living costs can be an overwhelming stress on the person diagnosed with this life-threatening disorder. Once the acute condition has been stabilized, nurses are often called on to provide counseling and to act as an advocate for the person with HF who is attempting to return to work. The purpose of this article is to review the literature on return to work and to offer suggestions for the nurse who is treating persons with HF. It is recommended that nurses be prepared to assess patients with HF, to provide resources, and to act as an advocate as needed. Further research is needed on the safe and effective transition of persons with HF into the workforce.

Intestinal obstruction mimicking acute myocardial infarction.

A 64-year-old woman presented at our institution with abdominal pain. An electrocardiogram suggested the possibility of acute anteroseptal myocardial infarction. Her medical history included esophageal reconstruction with use of a jejunal conduit in the anterior mediastinum. Echocardiography revealed a distended jejunal conduit, which was compressing the right ventricle. Once the cause was identified, nasogastric suction was initiated and the symptoms and electrocardiographic changes resolved.