Exertion and Acute Aortic Dissection

Role of Exertion or Emotion as Inciting Events for Acute Aortic Dissection

Ioannis S. Hatzaras MD, Jesse E. Bible MD, George J. Koullias MD, Maryann Tranquilli RN, Mansher Singh MD and John A. Elefteriades MD
Section of Cardiothoracic Surgery, Yale University School of Medicine, New Haven, Connecticut.

It is well known that hypertension, aortic dilatation, and collagen disorders predispose to acute aortic dissection (AAD). The inciting events that precede the instant of AAD are incompletely understood.
One hundred seventy-five consecutive patients having AAD, treated at our institution during a 10-year period, were reviewed; 65 were women and 110 were men (mean age 61 years). The ascending aorta was affected in 110 patients, and the descending in 65. Information was collected using patients’ charts supplemented with direct telephone interviews. Ninety patients were contacted; 65 (24 women, 41 men, mean age 61 years, average aortic size 5.56 cm) could recall specific inciting events for their dissection. In 34 patients, the ascending aorta was involved and in 31 the descending. Eighteen patients (28%) had a positive family history of aortic disease, defined as having ≥1 first-degree relative with aortic disease (aneurysm or dissection). In 24 of the 90 patients contacted (27%), strenuous activity was identified as a clear precipitating factor before the acute onset of thoracic pain; in 36 of 90 (40%) severe emotional stress preceded the onset of dissection pain. Three dissections were iatrogenic. Two additional patients reported a severe exacerbation of chronic obstructive pulmonary disease before their acute onset of chest pain.
In conclusion, severe physical and emotional stress may precipitate AAD, presumably on the basis of a transient, severe hypertensive reaction.

The American Journal of Cardiology
Volume 100, Issue 9, 1 November 2007, Pages 1470-1472

Losartan decreased myocardial ischemia

Effect of Losartan in Treatment of Exercise-Induced Myocardial Ischemia

Giancarlo Longobardi MD (a), Graziamaria Corbi MD, PhD (a, b), Francesco Cacciatore MD (a), Pasquale Abete MD (c), Giuseppe Furgi MD (a), Dino Franco Vitale MD (a), Franco Rengo MD (a, c) and Nicola Ferrara MD (a,b)

a) Cardiology Division, Fondazione “Salvatore Maugeri,” IRCCS, Scientific Institute of Telese Terme, Telese Terme, Italy; b) Department of Health Sciences, School of Medicine, University of Molise, Molise, Italy; c) Department of Clinical Medicine, Cardiovascular and Immunological Sciences, “Federico II” University of Naples, Naples, Italy.

Because no controlled clinical studies are available about the possible role of angiotensin II receptor blockers in preventing effort myocardial ischemia, we evaluated the effect of angiotensin II receptor blocker/losartan in preventing exercise-induced myocardial ischemia in patients with coronary artery disease.
Twenty-four sedentary patients with chronic stable ischemia were prospectively randomized to 28 days (double blind) of losartan 100 mg or losartan placebo in 2 divided doses. In each patient the treatment was crossed over to the alternative regimen (28 days, double blind) after a 1-week placebo period (single blind). At the end of each phase a new exercise stress test was performed. At baseline, systolic blood pressure was significantly decreased after losartan 100 mg compared with losartan placebo. At submaximal exercise, systolic blood pressure and rate–pressure product were lower after losartan 100 mg administration compared with losartan placebo, and these findings remained significant at 1-mm ST depression and at peak exercise. Losartan 100 mg administration versus losartan placebo significantly delayed the time to 1-mm ST-depression onset and decreased ST-segment depression at peak exercise and time to recovery of ST-segment depression. Losartan 100 mg administration compared with losartan placebo was able to significantly increase exercise duration and maximal workload during exercise stress testing.
In conclusion, in our study, losartan decreased electrocardiographic parameters of myocardial ischemia in patients with coronary artery disease, suggesting a possible role of this drug in treatment of patients with effort myocardial ischemia.

The American Journal of Cardiology
Volume 100, Issue 10, 15 November 2007, Pages 1517-1521

Coronary syndromes: Treating depression

Treating depression may improve recovery of heart rate variability following coronary syndromes

Patients with depression appear to have an impaired ability to recover their heart rate variability following acute coronary syndromes such as heart attack, a factor that could increase their risk of coronary death, according to a report in the September issue of Archives of General Psychiatry, one of the JAMA/Archives journals. However, patients who are treated with antidepressants or whose mood lifts may experience more of an improvement in heart rate variability than those who are untreated or remain depressed.
Heart rate variability refers to the degree to which the heart rate changes from beat to beat in response to normal impulses. "Low heart rate variability predicts death after myocardial infarction [heart attack]," the authors write as background information in the article. "It is reduced in depressed compared with non-depressed patients after myocardial infarction and has been proposed to be a mediator of the increased mortality associated with depression." In non-depressed patients who have an acute coronary episode, heart rate variability drops and then recovers substantially but not completely during the next few months.
Alexander H. Glassman, M.D., of the Columbia University College of Physicians and Surgeons and the New York State Psychiatric Institute, New York, and colleagues measured heart rate variability in 290 depressed patients an average of three weeks after they were hospitalized for acute coronary syndrome, a term encompassing heart events such as heart attack. The patients were then randomly assigned to take either the antidepressant sertraline or placebo for 24 weeks. After 16 weeks, 258 patients returned for a second heart rate variability reading. The severity of each participants' depression and their clinical response to depression treatment also were measured on previously established scales.
At the beginning of the study, previous episodes of depression were associated with lower heart rate variability. At the 16-week follow-up visit, the depressed patients had recovered their heart rate variability more slowly than expected and some even experienced a decrease. Patients who took sertraline had a 9 percent increase in heart rate variability and patients who took placebo had a 10 percent decrease, compared with the 28 to 33 percent increase in recovery of heart rate variability observed in previous studies of non-depressed patients.
"Both sertraline treatment and symptomatic recovery from depression were associated with increased heart rate variability compared with placebo-treated and non-recovered post-acute coronary syndrome control groups, respectively, but this results primarily from decreased heart rate variability in the comparison groups," the authors write.
The mechanisms behind the relationship between heart rate variability, depression and cardiac death remain unclear, the authors note. "What is clear is that depression is associated with biological changes involving increased heart rate, inflammatory response, plasma norepinephrine, platelet reactivity, decreased heart rate variability and now absent post-acute coronary syndrome heart rate variability recovery, all of which is associated with life-threatening consequences. Understanding why these characteristics so strongly associate with depression is crucial to understanding the nature of depression itself," they conclude.
"From a clinician's point of view, patients with depression after myocardial infarction, especially those with prior episodes, should be both carefully watched and aggressively treated, because they are at an elevated cardiac risk and less likely to get better spontaneously."

September 04, 2007
JAMA and Archives Journals

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Dark chocolate induces coronary vasodilation

Dark Chocolate Improves Coronary Vasomotion and Reduces Platelet Reactivity

Andreas J. Flammer MD, Frank Hermann MD, Isabella Sudano MD, PhD, Lukas Spieker MD, Matthias Hermann MD, Karen A. Cooper MSc, PhD, Mauro Serafini PhD, Thomas F. Lüscher MD, Frank Ruschitzka MD, Georg Noll MD, and Roberto Corti MD
From Cardiovascular Center (A.J.F., F.H., I.S., L.S., M.H., T.F.L., F.R., G.N., R.C.), Cardiology, University Hospital Zurich, Zurich, Switzerland; Nestlé Research Center (K.A.C.), Lausanne, Switzerland; and Antioxidant Research Laboratory (M.S.), Unit of Human Nutrition INRAN, Rome, Italy

Dark chocolate has potent antioxidant properties. Coronary atherosclerosis is promoted by impaired endothelial function and increased platelet activation. Traditional risk factors, high oxidative stress, and reduced antioxidant defenses play a crucial role in the pathogenesis of atherosclerosis, particularly in transplanted hearts. Thus, flavonoid-rich dark chocolate holds the potential to have a beneficial impact on graft atherosclerosis.

We assessed the effect of flavonoid-rich dark chocolate compared with cocoa-free control chocolate on coronary vascular and platelet function in 22 heart transplant recipients in a double-blind, randomized study. Coronary vasomotion was assessed with quantitative coronary angiography and cold pressor testing before and 2 hours after ingestion of 40 g of dark (70% cocoa) chocolate or control chocolate, respectively. Two hours after ingestion of flavonoid-rich dark chocolate, coronary artery diameter was increased significantly (from 2.36±0.51 to 2.51±0.59 mm, P<0.01), p="0.01)." p="0.04)">

Dark chocolate induces coronary vasodilation, improves coronary vascular function, and decreases platelet adhesion 2 hours after consumption. These immediate beneficial effects were paralleled by a significant reduction of serum oxidative stress and were positively correlated with changes in serum epicatechin concentration.

November 5, 2007

http://circ.ahajournals.org/cgi/content/abstract/CIRCULATIONAHA.107.713867v1

Vegetarian diet - Diminishes the risk for heart disease

Vegetarian Basics
Melissa Stevens, MS, RD, LD, Nutrition Program Coordinator, Preventive Cardiology and Rehabilitative Services

Following a vegetarian dietary pattern is one of the best ways to minimize your risk for coronary heart disease.

Benefits of a Vegetarian Diet
Rich in grains, fruits, vegetables, legumes, nuts and seeds, a vegetarian diet provides a host of phytonutrients, dietary fiber, vitamins and minerals found to help fend off disease.

In addition to reducing heart disease risk, people who follow a vegetarian or plant-based diet enjoy the following health benefits:

• Reduced risk of hypertension (high blood pressure).
  
• Lower total and LDL cholesterol levels.
  
• Lower body weight and reduced risk for obesity.
  
• Reduced risk of certain cancers (like colon and breast).
  
• Less risk of diverticular disease and digestive disorders.
  
• Increased longevity.
  

Types of Vegetarian Diets
There are many types of vegetarian diets. Some are followed for personal, religious, humanitarian or environmental reasons. The following are just some types of vegetarianism:

Semi-Vegetarian: Will usually eat everything but red meat. Poultry is often excluded, but fish and dairy products are almost always included.

Lacto-ovo-vegetarian: Will eat all dairy products, including butter, cheese and eggs but no meat, poultry or fish.

Lacto-vegetarian: Will eat dairy products but no eggs, meat, poultry or fish.

Vegan: Eats only plant foods like cereals, grains, fruits, vegetables, nuts and seeds. Excludes all foods of animal origin, including foods that contain any ingredients derived from an animal.

http://www.clevelandclinic.org/