Clinical case

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Choice of medications — The choice of medications in patients with DHF is determined by two factors:

●Treatment of specific underlying processes such as hypertension or symptomatic coronary heart disease (CHD). Combined therapy may be warranted since hypertrophied hearts are more sensitive to the deleterious effects of ischemia on left ventricular (LV) relaxation than nonhypertrophied hearts [12]. (See "Pathophysiology of diastolic heart failure".)



●The possibly beneficial effect of the drug on the pathophysiology of DHF



An important caveat is that the patient who has LV diastolic dysfunction with a small, stiff LV chamber is particularly susceptible to excessive preload reduction, which can lead to underfilling of the LV, a fall in cardiac output, and hypotension. In patients with severe LV hypertrophy (LVH) due to hypertension or hypertrophic cardiomyopathy, excessive preload reduction can also create subaortic outflow obstruction.

For these reasons, diuretics or venodilators such as nitrates and dihydropyridine calcium channel blockers must be administered with caution. Careful attention is required for symptoms of ventricular underfilling such as weakness, dizziness, near syncope, and syncope.

Digoxin is generally not used in patients with DHF because systolic function is intact. The DIG ancillary trial, a parallel study to the DIG trial, evaluated the role of digoxin in patients with HF and a LV ejection fraction (LVEF) >45 percent [13,14]. At a mean follow-up of 37 months, digoxin had no effect on all-cause or cause-specific mortality, or all-cause or cardiovascular hospitalization [13]. (See "Use of digoxin in heart failure due to systolic dysfunction".)

Antihypertensive therapy — Lowering the systemic blood pressure was associated with reduced rate of HF in some large randomized hypertension treatment trials, particularly those including diuretic therapy [15,16]. The choice of a specific antihypertensive agent must be individualized in the presence of coexisting diseases such as diabetes mellitus or chronic obstructive pulmonary disease. (See "Choice of drug therapy in primary (essential) hypertension: Recommendations".)

Regression of LVH is an important therapeutic goal, since it may improve diastolic function [17]. A meta-analysis published in 2003 attempted to evaluate the relative efficacy of different antihypertensive drugs for their ability to reverse LVH in patients with hypertension [18]. Eighty trials that included 146 and 17 active treatment and placebo arms, respectively, were evaluated. After statistical adjustments for length of therapy and degree of blood pressure lowering, the relative reductions in LV mass index were (figure 1):

●Angiotensin II receptor blockers (ARBs) - 13 percent

●Calcium channel blockers - 11 percent

●Angiotensin converting enzyme (ACE) inhibitors - 10 percent

●Diuretics - 8 percent

●Beta blockers - 6 percent



It appears that ARBs, calcium channel blockers, and ACE inhibitors produced more regression than beta blockers. The clinical significance of this difference is uncertain since there is as yet no evidence that more rapid regression of LVH is associated with improved long-term outcomes. The choice of antihypertensive therapy is usually based upon other factors.

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45 yo male in pre-op clinic for upcoming lap chole. Hx of HTN and DM. >4 METS. BP controlled 130s/70s. Normal physical exam. Approx 200lb. Pre-op EKG shows LVH. Further questioning of pt and review of old records shows worked up by cardiology approx 7 yrs ago. Echo at that time showed concentric LVH, normal EF, no LVOT obstruction or SAM. Negative stress test at that time as well. Pt was cleared by cardiology at that time for deployment (prior soldier) and note stated that he had a mild form of hypertrophic cardiomyopathy that had a very good prognosis and would not be limiting to pt in any way. EKG from 2007 apparently consistent with EKGs from 1990s per cards note, but none are available for review.

How do you proceed?

If it makes a difference, facility is a small community hospital (essentially an out patient surgery center). No ICU (step down only), cardiology, TEE, etc.

Thanks for posting Neo.

So how did the case pan out? Was there something lingering in the shadows or was it a straight forward case?
 
Good posts blade. I feel that diastolic dysfunction is often overlooked yet carries significant clinical predictability if you are on the restrictive side of things.

For the med studs learning this stuff, the graphs presented by blade were TTE and not TEE.
 
J Am Coll Cardiol. 2004 Oct 6;44(7):1446-53.
Outcomes in heart failure patients after major noncardiac surgery.
Hernandez AF1, Whellan DJ, Stroud S, Sun JL, O'Connor CM, Jollis JG.
Author information

Abstract
OBJECTIVES:
The purpose of this study was to evaluate mortality and readmission rates of heart failure (HF) patients after major noncardiac surgery.

BACKGROUND:
There is a lack of generalizable outcome data on HF patients undergoing major noncardiac surgery because previous studies have been limited to a few academic centers or have not focused on this group of patients.

METHODS:
Using the 1997 to 1998 Standard Analytic File 5% Sample of Medicare beneficiaries, we identified patients with HF who underwent major noncardiac surgery. A multivariable logistic regression model was used to provide adjusted mortality and readmission rates in patients after noncardiac surgery. Patients with coronary artery disease (CAD) and all other remaining patients (Control) who had similar surgery served as reference groups.

RESULTS:
Of 23,340 HF patients and 28,710 CAD patients, 1,532 (6.56%) HF patients and 1,757 (6.12%) CAD patients underwent major noncardiac surgery. There were 44,512 patients in the Control group with major noncardiac surgery. After accounting for demographic characteristics, type of surgery, and comorbid conditions, the risk-adjusted operative mortality (death before discharge or within 30 days of surgery) was HF 11.7%, CAD 6.6%, and Control 6.2% (HF vs. CAD, p < 0.001; CAD vs. Control, p = 0.518). The risk-adjusted 30-day readmission rate was HF 20.0%, CAD 14.2%, and Control 11.0% (p < 0.001).

CONCLUSIONS:
In patients 65 years of age and older, HF patients undergoing major noncardiac surgery suffer substantial morbidity and mortality despite advances in perioperative care, whereas patients with CAD without HF have similar mortality compared with a more general population.
 
You guys are not serious are you?
We are talking about a routine lap choly in a patient who is ASYMPTOMATIC who has GOOD EXCERCISE TOLERANCE!
All that crap mentioned above is irrelevant!
 
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You guys are not serious are you?
We are talking about a routine lap choly in a patient who is ASYMPTOMATIC who has GOOD EXCERCISE TOLERANCE!
All that crap mentioned above is irrelevant!

Plank. I don't think anyone is saying to delay this case.
Diastology and HOCM are good topics to discuss however.

45 yo male in pre-op clinic for upcoming lap chole. Hx of HTN and DM. >4 METS. BP controlled 130s/70s. Normal physical exam. Approx 200lb. Pre-op EKG shows LVH. Further questioning of pt and review of old records shows worked up by cardiology approx 7 yrs ago. Echo at that time showed concentric LVH, normal EF, no LVOT obstruction or SAM. Negative stress test at that time as well. Pt was cleared by cardiology at that time for deployment (prior soldier) and note stated that he had a mild form of hypertrophic cardiomyopathy that had a very good prognosis and would not be limiting to pt in any way. EKG from 2007 apparently consistent with EKGs from 1990s per cards note, but none are available for review.

How do you proceed?

If it makes a difference, facility is a small community hospital (essentially an out patient surgery center). No ICU (step down only), cardiology, TEE, etc.

So whats the ending to this story neogenesis?
 
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