Heart Failure

Overview of Congestive Heart Failure

E. Balbona M.D.

The effective treatment of heart failure goes back 200 years to William Withering’s introduction of digitalis, obtained from foxglove leaves. William Withering conducted his practice, in England in 1875, where he collaborated closely with medical and non-medical colleagues who were pioneers of intellectual thought during the industrial revolution. Because of his profound botanical knowledge, he was able to identify Digitalis purpurea as the essential ingredient in a prescription dispensed by a herbalist, and systematically proceeded to show its value in patients with cardiac failure.

1992 SAVE Study – Eugene Braunwald, M.D. (Harvard Univ) Left ventricular dilatation and dysfunction after myocardial infarction are major predictors of death. In experimental and clinical studies, long-term therapy with the angiotensin-converting—enzyme inhibitor captopril attenuated ventricular dilatation and remodeling. Within 3 to 16 days after myocardial infarction, 2231 patients with ejection fractions of 40 percent or less but without overt heart failure or symptoms of myocardial ischemia were randomly assigned to receive double-blind treatment with either placebo (1116 patients) or captopril (1115 patients) and were followed for an f 42 months.

Conclusions: In patients with asymptomatic left ventricular dysfunction after myocardial infarction, long-term administration of captopril was associated with an improvement in survival and reduced morbidity and mortality due to major cardiovascular events. These benefits were observed in patients who received thrombolytic therapy, aspirin, or beta-blockers, as well as those who did not, suggesting that treatment with captopril leads to additional improvement in outcome among selected survivors of myocardial infarction. (N Engl J Med 1992;327

1996 Carvedilol Study – Cohn J (Columbia Univ.)

N Engl J Med. 1996 May 23;334(21):1349-55.

The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. Controlled clinical trials have shown that beta-blockers can produce hemodynamic and symptomatic improvement in chronic heart failure, but the effect of these drugs on survival has not been determined. METHODS: 1094 patients with chronic heart failure in a double-blind, placebo-controlled, stratified program, in which patients were assigned to one of the four treatment protocols on the basis of their exercise capacity. Within each of the four protocols patients with mild, moderate, or severe heart failure with left ventricular ejection fractions < or = 0.35 were randomly assigned to receive either placebo (n = 398) or the beta-blocker carvedilol (n = 696);

Carvedilol therapy was accompanied by a 27 percent reduction in the risk of hospitalization for cardiovascular causes (19.6 percent vs. 14.1 percent, P = 0.036), as well as a 38 percent reduction in the combined risk of hospitalization or death (24.6 percent vs, 15.8 percent, P < 0.001). Worsening heart failure as an adverse reaction during treatment was less frequent in the carvedilol than in the placebo group.

Conclusions: Carvedilol reduces the risk or death as well as the risk of hospitalization for cardiovascular causes in patients with heart failure who are receiving treatment with digoxin, diuretics, and an angiotensin-converting-enzyme inhibitor.

1999, RALES Study – Pitt Bertram (Univ of Mich) Randomized Aldactone Evaluation Study.

The Randomized Aldactone Evaluation Study (RALES) was organized to explore the role of combination therapy with spironolactone in patients with heart failure. Patients with New York Heart Association Functional Class II-IV heart failure and left ventricular ejection fractions < or = 40% who were on regimens comprising an ACE inhibitor, loop diuretic, and, possibly, digoxin were randomized to receive placebo or spironolactone in doses of 12.5, 25, 50, or 75 mg per day. Even at the lowest dose of spironolactone, a significant decrease in plasma N-terminal pro-atrial natriuretic peptide occurred.. The RALES Mortality Trial will follow up 1400 similar patients for 3 years to determine the effect of the addition of spironolactone on combined mortality and hospitalization for heart failure.

RALES was a double-blind study which enrolled 1.663 patients with severe heart failure and a left ventricular ejection fraction of no more than 35 percent who were being treated with an angiotensin-converting-enzyme inhibitor, a loop diuretic and, in most cases, digoxin. A total of 822 patients were randomly assigned to receive 25 mg of spironolactone daily and 841 to receive placebo. The primary end point of the study was death from all causes. The trial was discontinued early after a mean follow-up of 24 months because an interim analysis determined that spironolactone was efficacious. There were indeed 386 deaths in the placebo group (46%) and 284 in the spironolactone group (35%) (relative risk of death: 0.70; 95% confidence interval, 0.60-0.82; p < 0.001).

Conclusions: The 30% reduction of mortality among patients in the spironolactone group was attributable to a lower risk of sudden cardiac death and of death from progressive heart failure. Patients treated by spironolactone had a lower hospitalization rate for worsening heart failure; they also had a significant improvement in the symptoms of heart failure as assessed by the New York Heart Association functional class.

Bone Health

Osteoporosis Screening

Eduardo J. Balbona, M.D.

Millions of American women have osteoporosis. These women are at risk for pathologic fractures leading to pain, deformity, disability and even death. Simple, inexpensive, rapid and reliable screening tests are avail­able, yet less than 10% of osteoporotic individuals are aware of their diagnosis. Several effective interventions are proven to reduce complications, yet less than half of the women at risk have even discussed osteoporosis with their physician. An estimated 28 million American women have osteopenia or osteoporosis and these num­ bers threaten to explode with current demographic trends (Figure 1). The direct medical expenses associ­ated with osteoporotic fractures approach $14 billion dollars annually and the indirect costs are staggering. A quarter of individuals will require long term nursing home care following a hip fracture and only 1 in 3 of those affected will ever regain their level of pre-fracture independence.

The gradual decline in bone density with age means that all one requires to develop os­teoporosis is simply to live long enough. The timely detection and institution of preventive measures must be the foundation of any effective osteoporosis manage­ ment program.

Bone mineral density (BMD) is the accepted surrogate for osteoporotic fracture risk. Bone density is a better predictor of fractures than blood pressure is of strokes or cholesterol is of heart attacks. Bone mineral density is felt to account for 80% of the variance in bone strength and resistance to fracture. Peak adult bone mass (PABM) is reached in both genders near age thirty. From that point onward, bone mineral density steadily declines. (Figure 2) The risk of fracture doubles with each standard deviation below peak adult bone mass (Table 2). The World Health Organization (WHO) bas defined osteoporosis as a bone density below 2 .5 standard deviations the mean BMD of young healthy adults.These alarming statistics demand the renewed com­mitment of the medical community to a program of increased public awareness, patient education, wide­ spread screening and regular monitoring of fracture risk

Osteoporosis qui­etly progresses without symptoms until late stage complications oc­cur (Table 1). Without proactive screening , os­teoporosis may go undetected and unchecked for years although it is a largely preventable.

Osteopenia or low bone density is defined as a BMD reduced between 1.0 to 2.5 standard deviations relative to this BMD. Normal bone density is defined as within 1 standard deviation of the mean young adult BMD. Bone density may now be determined via several modali­ ties from quantitative computed tomography (qCT) to dual energy x-ray absorptiometry (DEXA) or peripheral ultrasound measurement. Each modality has been shown to be independently predictive of fracture risk, yet each has it’s own limitations and results may not be compa­rable between modalities.

Quantitative computed tomography may be the most accurate and sensitive means of determining bone mineral density. The qCT exam measures the density of a three dimensional area of interest. This can be used to isolate the trabecular bone that is the most metabolically sensitive. Nevertheless, the applicat1on of qCT has been somewhat limited because of the added expense and radiation exposure as compared to alternatives. One alternative,dual x-ray absorptiometry (DEXA) measures the difference in absorption of low energy and high energy photons passing through tissues. The two dimen­ sional result is more likely to be influenced by overlying or nearby structures such as vascular or ligamentous calcifications or bony osteophytes. This may lead to artificially elevated and inaccurate results especially in the case of spinal measurements. For this reason, when there are discrepancies between the spinal and femoral BMD measurements, the femoral value may be more accurate. Finally, peripheral ultrasound of the calcaneus measures broadband ultrasound attenuation (BUA) and the speed of sound (SOS) through this weight bearing area. There is a high level of correlation between these values and bone mineral density as well as between calcaneal and central BMD. The ease of use, non­ invasive and cost effective qualities of the peripheral ultrasound have made it useful as an initial screening tool. However, an abnormal peripheral BMD screen should always be followed by a central BMD exam, be it qCT or DEXA based.

All women should be evaluated for osteoporotic risk in the same manner other medical risk factors are reviewed . Modifiable and non-modifiable risk factors should be discussed and will drive the need for further testing (Table 3). Non-modifiable risk factors include: female gender, Caucasian or Asian race, family history and a personal history of fracture as an adult. Modifiable factors include: smoking, inadequate dietary calcium, estrogen deficiency, excess dietary sodium, alcoholism, low body weight (<127 lbs), inactivity and lack of weight bearing exercise. Secondary causes of osteoporosis include a broad range of diseases and medications. Culprit medications may include corticosteroids, anticonvulsants, heparin, aluminum and thyroxine. Medical conditions associated with secondary osteoporo­sis include hyperparathyroidism, hyperthyroidism, dia­betes, chronic renal failure, scoliosis, gonadal insufficiency, multiple myeloma, lymphoma, chronic obstructive pulmonary disease, rheumatoid arthritis, sarcoidosis, and malabsorption syndromes among sev­eral others.

The bone mineral density of any patient is the product of their own personal history and part of a predictable lifelong process of skeletal development and deteriora­tion. The accepted WHO guidelines for osteopenia and osteoporosis compare peak adult bone mass (PABM) to a population of postmenopausal Caucasian women from the United Kingdom and the United States. About a third of all postrnenopausal women meet the WHO criteria for osteoporosis and half of these women will already harbor objective evidence of osteoporotic fractures. The WHO criteria simply provide a yardstick for comparison and allow for the identification of individuals at increased risk of osteoporotic fractures. The applicability of the WHO criteria to other ethnic groups or even premenopausal women has been the source of some debate. There are concerns regarding the possibility of exces­sive diagnosis, treatment and expense in otherwise low risk individuals. The incidence of osteoporotic fracture inpremenopausal females is indeed quite low and the lack of support for short-term interventions is not unex­pected. Nevertheless , the 30 or 40 year-old female with low bone mineral density is likely to eventually be the same 50 or 60 year-old individual who is at considerable risk from her now even lower BMD. The intervening years are ones of steady declines in bone mineral density in all clinical studies without exception.

In general, women lose about 1% of their spinal bone density per year. Thus the natural history of bone mineral density supports the need for screening at a stage when actual fracture risk is quite low. The potential benefits from early intervention are significant and it is important to note that even small changes in bone density can have dramatic benefits on the risk of fracture and long term complications. (Table 1)

Indeed, far from being viewed as a geriatric disease, osteoporosis has its roots in childhood and adolescence. Family practitioners and pediatricians increasingly rec­ ognize their responsibility to promote bone health at the stage oflife when the peak adult bone mass (PABM) can be readily affected. Children are susceptible to many conditions that interfere with normal bone development such as eating disorders and nutritional deficiencies . It is estimated that only ten percent of young girls ages 9 to 17receive adequate dietary calcium intake and many lack regular weight bearing exercise. Furthermore , chronic medications such as steroids and anticonvulsants may have profound effects on bone development and eventual adult peak bone mass.

Beyond the universal recommendations of the National Osteoporosis Foundation (Table 4) there are now several therapeutic options for intervention. They include estro­gen, progesterone, hormone replacement, raloxifene, tamoxifen, phytoestrogens, alendronate, risedronate, etidronate, and calcitonins with many more to come. Patients and their physicians need not passively await a future of isolation, deformity and disability from osteoporosis. Aggres­sive patient education and preventive measures should lessen the incidence and severity of osteoporosis in our communities.

Physi­cians should do what they do best – look into the future of their patients and take an active role in ensuring it is a long and healthy one.


I . National Osteoporosis Foundation : Physician Guide to Prevention and Treatment.of Osteoporosis: 1998.

2. Miller P. Clinical Application ofBone Densi tometry.Journal FMA .2000 ; 86:11-17 .

3. Lassanke P. Project Osteoporosis. Journal FMA. 2000; 86:33-34.

4. . Ullom-Minnich P. Prevention of Osteoporosis and Fractures. American Family Physician. 1999; 60: 194-201.

5. Andrews W. What ‘s cw in Preventing and Treating Osteoporosis. Postgrad uate Medicine. 1998; 104:89-97.

6. Vardy M, Cosman F. An Update on Osteoporosis. The Female Patienr. 1999; (September): 19-24.

7. Tonnino R. New tools for Osteoporosis Screening and Treatment Cleveland Clinic Journal of Medicine. 1998; 65:398-404.

8. Bier M, et al. Management of Osteoporosis and Risk Assessment. Clinical Geriatrics. 1998; 6(supp A):1- 16.

9. Khosla S, Riggs B. Treatment Options for Osteoporosis. Mayo Clinic Proceedings. 1995; 70:978-982.

10. DiMuzio M. The Revolution in Osteoporosis. Advance April 2000.

Early Detection

E.J. Balbona, MD,1

J.T. Balbona2

1Art of Medicine PA, Jacksonville
2Medical Student, Morsani College of Medicine, University of South Florida, Tampa

Address Correspondence to:

E.J. Balbona, MD
2257 Oak Street, Jacksonville, FL 32204
Email: ebalbona@bellsouth.net
Phone: 904-388-9202


Coronary artery disease (CAD) is a chronic condition that too often presents as a crisis of chest pain, heart attack or even sudden death. CAD begins in early adulthood and progresses silently over decades of life. Once identified it can be interrupted, hence the value of screening for silent, asymptomatic and subclinical disease. Half of all cardiovascular deaths occur in persons who were incorrectly assessed as low risk. Thus, it is imperative that physicians are aware of the importance of screening and the strengths and limitations of available cardiac tests including the Coronary Artery Calcium Score and the Nuclear Stress Test.


Two non-invasive cardiac testing modalities are commonly employed in the assessment of coronary artery disease: the Nuclear Stress Test (NST) and Coronary Artery Calcium Score (CAC). Their respective strengths and limitations should be considered in the evaluation of asymptomatic patients with possible coronary artery disease. The test characteristics of positive predictive value (PPV) and negative predictive value (NPV) are clinically relevant to the proper use of cardiac testing modalities.

The Nuclear Stress Test (NST) is limited by a low sensitivity and low positive predictive value (PPV) and is not optimal for screening asymptomatic or low risk patients. The Coronary Artery Calcium Score (CAC) with a high negative predictive value (NPV) is a useful screening tool for an asymptomatic and a low or intermediate risk patient. The CAC has other unique characteristics that make it useful for early identification, risk assessment, prognosis and promoting patient compliance in the management of coronary artery disease.

Cardiovascular disease (CVD) remains the number one cause of death globally.1 In the United States (U.S.), CVD kills 600,000 individuals every year and is the leading cause of death for both men and women.2 Several traditional risk factors are well known to increase the risk of cardiovascular disease. These factors include smoking, high blood pressure, elevated cholesterol, diabetes and family history.3 Physicians have actively sought out these factors to assess an individuals’ cardiovascular risk as well as to lower their risk of complications such as heart attack or stroke.4 Once identified, simple treatments such as lipid-lowering therapy can significantly lower the risk of complications.5,6 The challenge physicians face in diagnosing CVD is the high incidence of silent or unrecognized CVD with half of all cardiovascular deaths occurring in persons who are assessed as low risk.7 Many of the fatalities attributed to CVD were not optimally treated in the U.S. because the disease is unrecognized. Consensus ACC/AHA/ACP statements have noted that the “detection and treatment of risk factors can slow progression of atherosclerosis… and reduce the occurrence of clinical cardiovascular events in both primary and secondary prevention settings. More recently, it has been shown that atherosclerosis can be stabilized or even modestly reversed.”3

Currently, the Framingham Risk Assessment establishes a baseline for determining cardiovascular risk. Coronary Artery Disease (CAD) is an important category of CVD involving the buildup of plaque within the coronary arteries of the heart itself. It is important to establish a diagnosis of coronary artery disease in a stable asymptomatic patient when such a diagnosis does not exist. The early identification of coronary artery disease would often alter therapy and afford clinical benefit to the patient.

Physicians employ specific cardiac testing modalities in patients to further assess their cardiovascular status and future risks. Understanding the strengths and weaknesses of each testing modality is key to their effective use in clinical practice. Two non-invasive cardiac testing modalities are commonly employed in the assessment of coronary artery disease: the NST and CAC. Their respective strengths and limitations should be considered in the evaluation of asymptomatic and symptomatic patients with possible coronary artery disease.


Nuclear Stress Test (NST)

The Nuclear Stress Test is a means of determining which patients do not have high grade coronary obstructive disease with a negative predictive value (NPV) of 90 to 99 percent.8,9 The negative predictive value describes the strength of the tests’ negative result in the population studied. The NST is especially useful in the symptomatic patient in the setting of a high prevalence of coronary artery disease. The NST uses a radioactive analog that is associated with metabolic activity. Changes in blood flow within the heart at rest and with exertion are seen by measuring the level of radiation within the heart muscle using an external detector. Areas with lower radiotracer activity suggest blockages in the coronary arteries that supply that part of the heart. Other factors such as overlying gastric contents or breast tissue unfortunately may confound the test, producing a false positive result.

The NST is very limited for the evaluation of low-risk, asymptomatic patients with a positive predictive value (PPV) of as low as 12 percent.10,11

The NST is indicated in the assessment of intermediate or high-risk patients. Nevertheless, it is often used in clinical practice in lower risk populations and is poorly suited to this.10,11 If the NST is used in a low risk population, such as pre-operative patients, the likelihood of “false-positive” results will be much higher. This is reflected in the low PPV for the NST.10,11 The Nuclear Stress Test is thus of limited utility in a low risk population or as a screening method for coronary artery disease.

Coronary Artery Calcium Score (CAC)

The Coronary Artery Calcium Score is an objective means of determining which patients do not have coronary artery disease with a negative predictive value of 96 to 99 percent.11 Thus, it is an excellent screening tool for an asymptomatic or low-risk patient and a means of “ruling-out” coronary artery disease. The CAC uses a very low dose of radiation (1mSv) with a computerized tomography (CT) scan that is synchronized to the heartbeat to obtain images without motion artifact. It then measures the amount of calcified hard plaques within the coronary arteries of the heart. The presence of these calcifications correlates with the atherosclerotic burden present. A zero score provides your patient with the best prognosis of any cardiac test including coronary catheterization. When the calcium score is zero, it has both a high sensitivity of 99 percent as well as a high negative predictive value of 99 percent. This makes a score of zero the most clinically useful result of the heart calcium scoring exam.12 (Figure 2)

However, the CAC is a poor test for determining which patients do have flow limiting high-grade obstruction. The bulk of calcification seen on calcium scoring is subendothelial and resides within the arterial wall.13 It should not be confused with the acute intraluminal thrombosis of acute coronary syndromes.[i] Nevertheless, the coronary calcium score is useful in the diagnosis and clinical management of stable coronary artery disease.

The Tests in Use

The current workhorse of cardiac testing is the NST. The major limitation of the NST is its limited sensitivity and specificity of 80 to 85 percent,9 as well as the tests’ inability to detect non-occlusive coronary disease. Due to its limited sensitivity, up to 20 percent of NST negative results can be false negatives. In these patients with false negatives, there exists undetected obstructive coronary disease. These patients have an annualized rate of heart attack or death of 0.8 percent, or an 8 percent 10-year risk.14 Furthermore, the NST exam is unable to detect non-occlusive coronary disease. Patients with non-obstructive disease have a risk of death or myocardial infarction that is higher than those without CAD, estimated at 1.4 percent over ten years.14

A subsequent CAC test often confirms coronary disease in those individuals with negative NST results. In this setting, the heart calcium score is a complementary test to the NST. The CAC score has a negative predictive value of 99 percent. If the calcium score is zero, the patient’s chance of a cardiac death in the next decade is indeed very low (0.4 to 0.6%). Conversely, if the CAC score is very high, aggressive medical management is indicated. Large observational studies have shown 10-year survival in asymptomatic patients with coronary artery disease was 99.4 percent if the CAC score was 0 but was only 87.8 percent in those with a CAC score of greater than 1000.15 Several studies have confirmed the value of CAC scoring for assessing the risk of future cardiac events.16 A study of 8,425 men without clinical CVD from 1998-2007 evaluated those who underwent a preventive examination that included a measurement of CAC.17 In this cohort, the annual risk of a cardiovascular event was only 0.1 percent in those with a CAC of zero and almost 2 percent in those with CAC values ≥400.17 This twenty-fold increase in risk far exceeds the two to three-fold risk increase represented by traditional cardiovascular risk factors such as high cholesterol, hypertension or diabetes. The powerful prognostic measure of CAC can be adjusted for age, gender and ethnicity to identify individuals at high CVD risk who would benefit from aggressive primary prevention with medical management.18,19 Studies have demonstrated that statin-based lipid-lowering therapy can slow or even reverse the progression of atherosclerosis seen on coronary calcium scoring.20

In the acute setting, a NST or Left Heart Catherization may be necessary to ensure patient safety. In the future, the coronary CTA (CT Angiogram) or MRA (MR Angiogram) tests will likely impact this use of the NST. There are also refinements to the calcium score such as measures of calcium volume and density that promise to further increase the predictive value of calcium scoring. Notably, calcium density is inversely related to CV risk and may reflect plaque stabilization and the healing process within the arterial wall.22 More densely calcified plaque appears to contribute less to cardiovascular events and may be more resistant to plaque rupture.22 Additionally, the newer lesion specific calcium scoring (Voros method) has been shown to better predict the presence of obstructive coronary artery disease compared to the traditional Agaston calcium score.23 The Agaston score is the standard semiautomated method of assessing a calcium score value. The Agaston score is the weighted density score given to the highest attenuation value or “Hounsfield units” (HU) greater than 130 that are then multiplied by the area of the calcification. Many studies have shown that the Agaston score affords a method of risk stratification with a stepwise increase in risk with higher Agaston score.

Grading of Agaston scores is as follows:

No evidence of CAD: 0

Minimal CAD: 1-10

Mild CAD: 11-100 Moderate: 101-400

High Risk: >400

These values are proven to be predictive of the risk for future major adverse cardiac events.24 It should also be pointed out that the positive and negative predictive value of any test is influenced by the prevalence of disease in the population. The values of PPV and NPV are clinically relevant since the consideration of the disease prevalence and test predictive power is fundamental to the proper use of cardiac testing modalities. The clinical setting of pre-test probability and the symptomatic versus asymptomatic patient also inform which tests are best suited to the question at hand. The use of appropriate testing modalities should afford better differentiation regarding which patients should and which should not require invasive procedures. A screening test result alone should never lead to an invasive procedure that could place a patient at risk; rather, it should inform the physician as to their patient’s condition. The cardiac calcium score has other unique characteristics. Although many physicians only assess a calcium score as a numeric value, the review of the images of coronary plaque is invaluable. The coronary calcium score comes with a compact disk that will play on most computers. Viewing the plaque within each of the coronary arteries with the patient provides overwhelming visual evidence and compels the patient into an active prevention and treatment mindset. The CT scan images demonstrate bright white hard calcium deposits within the heart that often shock patients from their denial of disease. A meta-analysis of studies with over 11,000 patients has shown a two to three-fold increase in initiation of aspirin, lipid-lowering and anti-hypertensive medications as well as lifestyle changes for those with evidence of coronary calcium compared with patients having none.25 (Figures 1-8)

Figures 1-8: Examples of CAC Images

Figure 1: Proximal Left Anterior Descending Artery calcification demonstrated. The calcium score for this artery alone was 250 per Agaston technique.

Figure 2: Right Coronary Artery without calcification and calcium score of zero is free of calcified plaque.

Figure 3: Right Coronary Artery calcification demonstrated in patient with total CAC score over 1000. Note that calcification involves arterial wall seen in cross section here.

Figure 4: Left Circumflex Artery calcification demonstrated bottom right with score for this artery of 90. Note the normal non-calcified Right Coronary Artery seen at top left.

Figure 5: Left Anterior Descending Artery calcification demonstrated in a patient with mild coronary artery disease with a CAC score of 85.

Figure 6: Proximal Left Anterior Descending Artery calcification is demonstrated in patient with total CAC score of 700.

Figure 7: Proximal Right Coronary Artery calcification demonstrated in patient with RCA calcium score of 900. Note that the sternum is seen at top of image and spine at the bottom. There is also a small area of calcified plaque seen in the wall of the descending aorta. The bright white character of the areas connotes the relative high density of the calcifications.

Figure 8: Left Main Coronary Artery arising from the Aorta with a calcified plaque in the proximal Left Anterior Descending Artery. The CAC score for the LAD is 250.

The CAC test may be of less value in the inpatient setting with symptomatic patients. This is typically where chest pain is evaluated and thus there is concern regarding soft plaque and acute obstruction not seen by calcification scoring. It also can be argued that coronary calcium scoring will prompt inappropriate use of left heart catheterization. These should be reserved for high-risk patients and medical management remains the most effective and safe intervention for all but those in acute coronary syndrome.26

The current problem facing physicians is not the over-diagnosis of cardiovascular disease but the opposite.27 Particularly in young men, there is ample evidence that traditional risk factors cannot adequately predict cardiovascular risk.28 Recent data from the Centers for Disease Control and Prevention (CDC)’s Million Hearts 2022 initiative suggest more should be done to identify cardiovascular disease in asymptomatic individuals.29 The findings suggest that as many as one in three hospitalizations and deaths related to cardiovascular events in 2016 involved adults in middle-age — between the ages of 35 and 64.

During a press briefing, the CDC’s Principal Deputy Director Anne Schuchat, MD stated, “many of these cardiovascular events are happening to middle-aged adults – who we wouldn’t normally consider to be at risk. Most of these events can be prevented through daily actions to help lower risk and better manage medical conditions.”29 The CAC provides high sensitivity and negative predictive values for identifying cardiovascular disease. Once appreciated in an individual, preventive measures proven to reduce cardiovascular mortality include the use of aspirin and statins, glucose and blood pressure control, as well as smoking cessation and regular exercise. CAC scoring can also be done at a very low cost similar to that of an EKG. The diagnostic and prognostic power of CAC scoring has been extremely well documented. A recent prospective study by Shaw et al of more than 63,000 asymptomatic patients who were followed over 12 years showed once again the superiority of CAC scoring to the Framingham Risk Score. For a calcium score of zero, keeping with the results of other studies, the observed CV mortality was very low in both men and women at 0.4% over the 12-year follow-up. However, with a calcium score of over 400, the hazard ratio for cardiovascular mortality increased dramatically to 9.1 or a nine times greater risk of cardiovascular death.30 These results far exceed the prognostic power of Framingham Risk Scores or of any other cardiac test currently available. Also, the risk from coronary calcification was found to be greater in women than in men.30


The Nuclear Stress Test is a useful cardiac testing modality for symptomatic patients and those patients at high risk for obstructive coronary artery disease. However, it is of limited utility in a low risk population or as a screening method for coronary artery disease.

The Coronary Artery Calcium Score is an underutilized test with a cost similar to an EKG that uses less radiation than a mammogram and takes only ten seconds of CT time. It offers useful information in the proper setting and in the hands of an informed physician. The CAC has other unique characteristics that make it useful for early identification, risk assessment, prognosis and promoting patient compliance in the management of coronary artery disease

If physicians truly intend to impact the unacceptably high morbidity and mortality of cardiovascular disease, its early identification and preventive care should be prioritized. The use of CAC data and CT images that are visually reviewed is a very powerful tool in educating physicians as well as personalizing the disease to the patient.30

A better understanding of cardiac testing modalities will ultimately lead to better care of patients. That is the shared goal of all physicians.


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2. CDC WONDER: Underlying Cause of Death 1999-2013 [Internet]. Atlanta (GA): U.S. Department of Health and Human Services. 1999 – 2013 [cited 2015 Feb 3]. Available from: https://wonder.cdc.gov/.

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16. LaMonte MJ, FitzGerland SJ, Church TS, et al. Coronary artery calcium score and coronary heart disease events in a large cohort of asymptomatic men and women. Am J Epidemiol. 2005 Sep 1;162(5):421–9.

17. Radford NB, DeFina LF, Leonard D, et al. Cardiorespiratory fitness, coronary artery calcium, and cardiovascular disease events in a cohort of generally healthy, middle-age men: results from the Cooper Center longitudinal study. Circulation. 2018 May 1;137(18):1888–95.

18. Detrano R, Guerci AD, Carr JJ, et al. Coronary calcium as a predictor of coronary events in four racial or ethnic groups. N Engl J Med. 2008 Mar 27;358(13):1336-45.

19. Bild DE, Detrano R, Peterson D, et al. Ethnic differences in coronary calcification: the Multi-Ethnic Study of Atherosclerosis (MESA). Circulation. 2005 Mar 15;111(10):1313-20.

20. Achenbach S, Ropers D, Pohle K, et al. Influence of lipid-lowering therapy on the progression of coronary artery calcification: a prospective evaluation. Circulation. 2002;106:1077–82.

21. DeWood MA, Spores J, Notske R, et al. Prevalence of total coronary occlusion during the early hours of transmural myocardial infarction. N Engl J Med. 1980 Oct 16;303(16):897-902.

22. Criqui MH, Denenberg JO, Ix JH, et al. Calcium density of coronary artery plaque and risk of incident cardiovascular events. JAMA. 2014 Jan 15;311(3):271-8.

23. Qian Z, Anderson H, Marvasty I, et al. Lesion- and vessel-specific coronary artery calcium scores are superior to whole-heart Agatston and volume scores in the diagnosis of obstructive coronary artery disease. J Cardiovasc Comput Tomogr. 2010 Nov-Dec;4(6):391–9.

24. Arad Y, Spadaro LA, Goodman K, et al. Prediction of coronary events with electron beam computed tomography. J Am Coll Cardiol. 2000 Oct;36(4):1253-60.

25. Gupta A, Lau E, Varshney R, et al. The identification of calcified coronary plaque is associated with initiation and continuation of pharmacological and lifestyle preventive therapies: a meta-analysis. JACC Cardiovasc Imaging. 2017 Aug;10(8)::833-42.

26. Boden WE, O’Rourke RA, Teo KK, et al. Optimal medical therapy with or without PCI for stable coronary disease. 2007 Apr 12;356(15):1503-16.

27. Akosah KO, Gower E, Groon L, et al. Mild hypercholesterolemia and premature heart disease: Do the national criteria underestimate disease risk? J Am Coll Cardiol. 2000 Apr;35(5):1178–84.

28. Berry JD, Lloyd-Jones DM, Garside DB, et al. Framingham risk score and prediction of coronary heart disease death in young men. Am Heart J. 2007 Jul;154(1):80-6.

29. Melville NA. Cardiovascular event rates high in middle age: CDC [Internet]. Medscape; 2018 Sep 11 [cited 2019 Jan]. Available from: https://www.medscape.com/viewarticle/901809

30. Shaw LJ, Min JK, Nasir K, Xie JX, Berman DS, Miedema MD, Whelton SP, Dardari ZA, Rozanski A, Rumberger J, Bairey Merz CN, Al-Mallah MH, Budoff MJ, Blaha MJ. Sex differences in calcified plaque and long-term cardiovascular mortality: observations from the CAC Consortium. Eur Heart J 2018;39:3727–3735.

Heart Health

Eduardo J. Balbona, M.D. 

Cardiovascular disease remains the leading cause of death and disability in the United States.  It is the product of atherosclerosis and ultimately leads to the complications of heart attack and stroke. Cardiovascular disease includes coronary heart disease, the cause of over a million heart attacks annually in the United States. Tragically, for up to a third of heart attacks victims, the first symptom will be sudden death. By the age of 40, the lifetime risk of developing coronary heart disease is one in two for American men and one in three for American women. (1).

“A common pathway to the expression of coronary heart disease is the presence of sub-clinical (pre-symptomatic) atherosclerotic disease. . .. Sub-clinical atherosclerosis may (now) be detected non-invasively by both physiologic and anatomic methods.”    Daniel Rader, M.D., The American Journal of Medicine. (2).

Medical research supports the concept of the identification of presymptomatic individuals to allow for prevention of cardiovascular events. Numerous medical studies have found that the development of atherosclerotic plaques begins in childhood or adolescence and then gradually progresses over several decades. Individuals will eventually become symptomatic with the development of a high-grade obstructing lesion (plaque), typically when the artery is over 70% blocked. The time course of cardiovascular disease allows ample opportunity for intervention in the disease process.

Common methods of cardiovascular disease detection and screening are based on the demonstration of symptoms or of significant blood flow obstructing lesions. Both of these findings occur late in the natural history of cardiovascular disease and are thus inadequate for the purposes of prevention . Almost 70% of deaths from heart attacks have culprit lesions associated with less than a 50% obstruction of the coronary artery. (3). These fatal lesions are considered “normal” or “insignificant” on heart catherization and coronary angiography. Instead of focusing on the “lesion” of interest, enlightened physicians should set out to find the “individual” of interest that would benefit most from medical intervention.

Secondary prevention studies, such as the Scandinavian Simvastatin Survival Study (4S) have proven the cost effectiveness of medical therapies such as cholesterol lowering in individuals with known atherosclerosis. (4) The 4S study demonstrated a 42% reduction in coronary deaths and a 37% reduction in the need for angioplasty or bypass surgery. Based on this study, in order to prevent one cardiovascular event (over 5.5 years) only 12 patients would need treatment as opposed to almost 120 patients that would require intervention (over 4.8 years) for the same result in the case of primary prevention (individuals with no atherosclerosis documented). (5).

 Non-invasive screening provides clinically pertinent information. Consider the fact that current national cholesterol education program (NCEP) guidelines will accept an LDL cholesterol of 220 mg/dL in a young adult. However, the same NCEP guidelines mandate medical intervention to maintain the LDL below 100 mg/dL once atherosclerosis is demonstrated. Furthermore, the earlier the intervention occurs, the greater the benefit. For example, a 10% reduction in cholesterol by age 40 yields over a 50% decline in the lifetime coronary heart disease risk, while only a 40% benefit if done at age 50 and only 27% if at age 60. (6)

Non-invasive documentation of atherosclerotic lesions is now possible and the case for screening for sub-clinical cardiovascular disease is compelling. Carotid ultra-sonography identifies the presence of atherosclerosis in the carotid arteries. The extent of carotid atherosclerosis has been shown to correlate with coronary plaque burden and is an independent risk factor for major cardiovascular events. (7).

The ankle-brachial index (ABI) is also a useful means of detecting peripheral atherosclerosis. Clinical studies have shown an abnormal ABI to be a predictor of coronary heart disease that justifies the institution of secondary prevention guidelines. (8). Similarly, prospective studies have demonstrated that cardiac calcification scores in asymptomatic individuals (via EBCT) are highly predictive of subsequent symptomatic coronary disease. (9).

“The key to reducing the risk of heart disease is to have a system in place to identify and treat patients that are at high risk. Currently, many people are not identified or are inadequately treated …” Harlan Krumholz M.D., cardiologist, Yale School of Medicine. ( 10)

The non-invasive identification of pre-symptomatic atherosclerosis transforms the physician’s role from one of reaction to a sudden cardiovascular crisis, to that of prudent pro-active prevention via medical management. Proven preventative measures include: anti-hyperlipidemic, anti-thrombotic, anti-inflammatory and anti-oxidant interventions as well as smoking cessation, strict blood pressure control and diabetes management.

Early identification of pre-symptomatic individuals with atherosclerotic lesions benefits not only the patient, but also the community, health system and employers that are no longer burdened with the consequences, complications and costs of advanced cardiovascular disease.


I . Loyd-Jones DM, Larson M, Beiser A, Levy D. Lifetime risk of developing coronary heart disease. (The Framingham Heart Study) Lancet. 1999; 353: 89-92.

2. Rader DJ. Noninvasive Procedures for Subclinical Atherosclerosis Risk Assessment. Proceedings of Symposium . The American Journal of Medicine. 1999; I 07: 25S-27S.

3. Rumberger JA, Brundage BH, Rader DJ, Kondos G. Electron Bean Computed Tomographic Coronary Calcium Scanning : A Review and Guidelines for Use in Asymptomatic Persons. Mayo Clinic Proceedings. 1999; 74: 243-252 .

4. Pederson , et al. Randomized Trial of Cholesterol Lowering in 4,444 Patients with Coronary Heart Disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994; 344: 1383-1389.

5. Brown BG. Assessment for Subclinical Ischemia: Bridging the Gap Between Primary and Secondary Prevention . Proceedings of Symposium. The American Journal of Medicine. 1999; 107: 28S-30S.

6. Kwiterovich PO. Young Adults with Hypercholesterolemia . Proceedings of Symposium. The American Journal of Medicine. 1999; I 07: 40S-42S.

7. O’Leary DH, Polak JF, Kronmal RA, Manolio TA, Burke GL, Wolfson SK, Carotid Artery intima and medial thickness as a Risk Factor for Myocardial Infarction and Stroke in older Adults: Cardiovascular Health Study Collaborative Research Group. The New England Journal of Medicine. 1999; 340: 14-22.

8. Grundy SM. Primary Prevention of Coronary Heart Disease: Selection of Patients for Aggressive Cholesterol Management. Proceedings of Symposium. The American Journal of Medicine. 1999; I 07: 2S-6S.

9. Arad Y, Spadaro LA, Goodman K, Lledo-Perez A, Sherman S, Lerner G, Guerci AD. Predictive Value of Electron Beam Computed Tomography of the Coronary Arteries: a 19-month study of 1173 asymptomatic subjects. Circulation. 1996; 93: 1951-1953.

10. Peterson C. Aggressive Cholesterol Management bests Heart Disease. Identifying and Treating Patients at High Risk and Suppressing LDL Might Stave Off Surgery. Managed Healthcare . 2000 : 41-42.

Smoking & Lung Cancer

Lung Cancer  Screening

Eduardo J. Balbona, M.D. 

Lung cancer is the most common form of cancer in the world. It is also the leading cause of cancer death for both men and women in America. There will be over 160,000 new cases of lung cancer diagnosed this year. The vast majority, almost 90%, will be associated with smoking or a history of smoking in the past. Tragically, the 5-year survival for these individuals diagnosed with lung cancer is only 12-14 percent. By the time symptoms appear or the individual feels ill, lung cancer is often far advanced. The diagnosis typically occurs too late for lung cancer to be effectively treated. Yet when detected early (in Stage 1) lung cancer survival rates are dramatically better, as high as 80-95% (5-year survival).

Early detection strategies are common for cancers of the breast, colon, and prostate. Although lung cancer will kill more Americans than all of these cancers combined, no early detection strategy for lung cancer is widely utilized. Recent studies have proven that the use of low dose Spiral Lung CT can detect four times the number of lung cancers as compared to traditional chest x-rays. Moreover, these cancers were six times more likely to be at the earliest stage (Stage 1) when the chances for cure are best.

The low dose Spiral Lung CT is painless, safe, rapid, and cost effective. The actual procedure requires only a few seconds and is a fraction of the cost of a traditional CT scans. The exam’s x-ray exposure in this procedure is minimal (it is safe) and there is no risk from medications or from intravenous contrast.

You should be aware that many nodules detected by CT are in fact non-cancerous. The presence of calcium in a nodule is an indication that it is very likely a benign granuloma (a scar). Also, even non-calcified nodules may not prove to be cancer and will require a physician’s prudent judgment to manage these appropriately. Your personal physician can use the information gathered by a low dose Spiral Lung CT to follow any abnormalities and take timely action when needed. Also, no test can substitute the need for a careful examination and the expert advice of your physician.

There is no better preventive measure you can do than to not smoke or to quit as early as possible. But if you or your loved one has a significant smoking history, then the use of low dose Spiral Lung CT examinations is an example of the many benefits of early detection and prevention.


The Strength of Good Nutrition

Eduardo J. Balbona, M.D. 

Which is stronger?

A board of oak or a single acorn?

A granite stone or your little finger?

Once in the ground, the board will decay while the acorn grows into a strong new oak tree. The wind and rain will grind the stone to dust, yet your hands and body can grow stronger each day. 

The difference is LIFE.

Life is the most powerful force on the planet. Life creates you anew, from your diet and your habits. Each day, you gradually create the person you will be tomorrow and years from now. All the atoms in your body are exchanged every few months. Your body is not simply a collection of static pieces but rather the constant flow of life moments that act on every atom, molecule, and every body part. The momentum of life springs from the information within every cell in your body, within every strand of DNA. The raw materials of your health lie in the choices you make each day, the foods you eat, your level of exercise, and the effects of your good as well as your bad habits.

What you eat matters.

Poor nutrition is a risk factor for heart disease, obesity, high blood pressure, stroke, elevated cholesterol, diabetes, respiratory problems as well as cancers of the breast, colon, and prostate. The body mass index (BMI) is simply a measure of the ratio of your weight relative to your height that is useful in gauging your weight status. The American Cancer Society conducted a 14-year study of one million adults and found that being overweight (a body mass index of 25 or higher) is associated with an increased risk of death from cardiovascular disease as well as cancer.

Goals of Healthcare

Goals of Primary Care Services:

We are here to serve you and work to safeguard and improve your health. This is only possible through a partnership of mutual understanding and respect.

These ten steps are the foundation of our basic goals for your care.

  • Hypertensive control – a blood pressure systolic of less than 130 systolic
  • Cholesterol/ Lipid control – a total cholesterol of less than 200 and an LDL of less than 130
  • Weight moderation – a BMI of less than 30 (i.e. non-obese)
  • Tobacco cessation – help you stop smoking
  • Alcohol moderation – less than one or two drinks daily
  • Healthful activity – exercise guided by your level of fitness
  • Stress reduction – counseling, meditation and meds if needed
  • Cancer Screening – colonoscopy, mammograms & testing as indicated
  • Disease Screening – glucose and thyroid levels, bone density etc.
  • Risk Factor elucidation – review of your personal and family history & risks

These are the steps we expect you to take.

  1. Compliance – taking your medications and treatments
  2. Vaccinations – all vaccines that are indicated
  3. Honesty and kindness – courtesy with all staff at all times

As a small practice we do have limits on the services we can provide and may have to refer to outside physicians for their added expertise. We believe in stable long-term relationships with a trusted physician as the best means of providing meaningful care.

Other clinics have large teams of physician extenders and providers to process patients through their systems rapidly and efficiently. This is not our approach. We trust you will appreciate the advantages of smaller and simpler primary care.

We look forward to the privilege of serving you for years to come.


Eduardo J. Balbona M.D. & Staff – Art of Medicine, PA


In “Open Your Eyes: A Prescription for Change in American Health Care,” Dr. Eduardo Balbona shares his expert advice on how U.S. health care can be improved from its current state, in which both patients and doctors are unable to thrive. Gleaned from his more than 30 years of practicing medicine, Balbona’s text illustrates how our ideas on medical care have developed, and ultimately at what cost. Along with providing engaging excursions into medical education and history, he also shares patient vignettes to show the human stories behind the evolution of medicine. Having served in many types of medical practices, including as a naval officer and U.S. Capitol physician,

Link to Amazon Bookstore. 


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