Cardiology

Despite meticulous titration of anticoagulation therapy and careful attention to confounding medications, serious bleeding complications occur in some patients who receive warfarin.

Some of my patients who are being treated for hypertension, hyperlipidemia, or both claim that an elevated blood pressure reading or lipid level measurement resulted from a sodium- or fat-laden meal that they had eaten 1 or 2 days before their office visit.

At what level should a patient's blood pressure be before he or she has carotid surgery?

Treatment of hypertension can minimize both microvascular and macrovascular complications of diabetes and helps prevent nephropathy and cardiovascular events.

Is there any relationship between hiccups and an implanted cardiac pacemaker? Could hiccups possibly trigger a change in the pacemaker?

Primary care practice is filled with patients who have acute coronary disease complicated by multiple comorbid conditions. In this era of percutaneous treatments, contrast-induced nephropathy persists as an unwelcome and debilitating complication.

A 44-year-old man presents to the emergency department (ED) with light-headedness, nausea, and vomiting of 1 day's duration. He has also had intermittent palpitations but denies chest pain, dyspnea, and weakness.

In his article, "Heart Failure: Part 1, Diagnosis and Staging" (CONSULTANT, July 2007), why did Dr W. H. Wilson Tang omit central venous pressure and circulation time as means of diagnosing congestive heart failure? Is it possible that the simplicity and accuracy of these 2 tests, which can establish the diagnosis in 5 or 10 minutes in any hospital room-or physician's examining room-have been forgotten since the advent of testing of natriuretic peptide levels (which, as Dr Tang notes, "also increase in response to other noncardiac processes")?

The development of more sophisticated testing modalities now permits the identification of coronary artery narrowing in asymptomatic adults. The images obtained in these studies provide potential targets for intervention-based therapy.

For 4 days, a 34-year-old pregnant woman had dyspnea and right-sided chest pain. She denied fever, chills, sweats, cough, lower extremity pain, and edema. Surgical and social histories were unremarkable. She was taking progesterone and clomiphene citrate for the past 6 months for assisted reproduction.

Over the past 20 years, the treatment armamentarium for diabetes has greatly expanded: 8 different classes of non-insulin drugs and 8 different types of insulin are now available. The newer classes of agents include disaccharidase inhibitors, thiazolidinediones, meglitinides, glucagonlike peptide analogs, and dipeptidyl peptidase IV inhibitors.

Forty-eight hours ago, a 39-year-old man presented to the emergency department with emesis and severe upper abdominal pain of semi-acute onset, which radiated slightly to the back.

A 63-year-old man with a history of hypertension and gastroesophageal reflux disease presented with progressive, sharp mid-abdominal pain of 3 weeks' duration.

Interatrial septal aneurysm (IASA) and patent foramen ovale (PFO)-either alone or coexisting-are a frequent cause of cryptogenic cerebral and/or peripheral thromboemboli. The IASA plus PFO combination has been shown to confer higher risk, particularly in adults aged 45 years or younger. Therefore, recognition and documentation of these 2 abnormalities during an echocardiographic (transthoracic or transesophageal) study, when performed for other indications, is essential.

I read with interest Dr Gregory Rutecki's response to a reader's comments (CONSULTANT, February 2007), in which he emphasized the need for early screening and treatment of cardiovascular disease in patients with chronic kidney disease (CKD).

A 68-year-old woman with hypertension complains of intermittent dyspnea and light-headedness. She is asymptomatic during the evaluation. Vital signs are normal, but an irregularly irregular pulse is noted on examination as well as on the telemetry monitor. The 12-lead ECG is shown here; the ECG machine printout reads "atrial fibrillation." The patient has no history of this arrhythmia.

Current evidence suggests that out-of-office blood pressure measurements and 24-hour ambulatory blood pressure monitoring are better predictors of cardiovascular risk than routine office measurements. Is it time to make greater use of automated devices in my practice?

My patient is an 82-year-old woman with a history of coronary artery bypass grafting (CABG), chronic obstructive pulmonary disease (COPD), pulmonary hypertension, and mild intermittent angina on exertion, which is relieved by sublingual nitroglycerin.

ABSTRACT: Angiotensin-converting enzyme inhibitors and ß-blockers are the cornerstone of heart failure medical therapy; unless contraindicated, start these agents as soon as possible after volume status has been optimized. Aldosterone receptor antagonists, angiotensin-receptor blockers, and a fixed-dose combination of hydralazine and isosorbide dinitrate (the last recommended especially for African Americans) can be used as add-on therapy. Prophylactic implantable cardioverter defibrillators reduce long-term mortality in symptomatic patients with a left ventricular ejection fraction (LVEF) of 35% or less. Cardiac resynchronization therapy improves symptoms and ventricular remodeling in some patients; indications include wide (more than 20 milliseconds) QRS complex on ECG, impaired LVEF (35% or less), and advanced heart failure symptoms (NYHA classes III and IV) despite optimal drug therapy. Measurement of natriuretic peptides and impedance cardiography both show promise for monitoring patients with heart failure and for guiding therapy, but definitive data to justify their routine use are still lacking.

Having suffered many assaults on my eardrums from patient vocalizations during auscultation for carotid bruits, I now ask patients to take a deep breath and hold it as I listen to the vessels in their neck.

At a routine blood pressure check, a 63-year-old woman has 2 readings of 165/100 mm Hg. The patient has had essential hypertension since age 41 years. For more than a decade, it was easily controlled with a b-blocker; however, in recent years, her blood pressure has been more variable, with occasional readings of higher than 150/90 mm Hg.

Heart failure is prevalent in both primary care and cardiology practices. It develops in about 1 in 5 persons during their lifetime and in about 1 in 8 of those who have not sustained a myocardial infarction (MI). Heart failure is also the leading cause of hospitalization in the elderly.

Lp(a) is a fascinating variant of low-density lipoprotein (LDL). It is basically an LDL molecule that has been modified by the covalent addition of apoprotein(a). Elevated levels of Lp(a) correlate with increased risk of acute coronary syndromes, cerebrovascular accident, peripheral arterial disease, and coronary mortality. This Q&A session answers some curiosities about Lipoprotein(a).

A 67-year-old woman arrived via ambulance in ventricular tachycardia. She had been experiencing crushing substernal chest pain and shortness of breath that had worsened over the past several hours. She received oxygen (by mask) and lidocaine (100 mg intravenously) en route to the emergency department (ED), but there was no change in the rhythm.

ABSTRACT: Atypical clinical presentations in the quality, intensity, and radiation of pain are common in patients with acute coronary syndromes. Women with an acute myocardial infarction (AMI) are more likely to have atypical symptoms, such as dyspnea, than men. A history of acute anxiety or a psychiatric diagnosis does not preclude the possibility of an acute coronary event in a patient with chest pain. The clinical response to a GI cocktail, sublingual nitroglycerin, or chest wall palpation does not reliably identify the source of pain. Over-reliance on tests with poor sensitivity, such as the ECG, or on the initial set of cardiac biomarkers will miss many patients with MI. Serial troponin levels obtained at 3- to 6-hour intervals are recommended to evaluate the extent of myocardial damage. Coronary angiography that detects mild non-obstructive disease does not exclude the possibility of sudden plaque rupture and acute coronary occlusion.